木丹颗粒治疗糖尿病并下肢动脉硬化闭塞症临床研究
|
摘要
糖尿病并下肢动脉硬化闭塞症（DLASO）作为糖尿病常见大血管并发症之一，近年来发病率逐渐升高，其临床表现轻者肢体麻、凉、疼痛、间歇性跛行，重者发展为坏疽，甚至截肢，严重影响患者的日常工作和生活。为此研究与该病发生、发展密切相关的危险因素，做到未病先防，既病防变，寻求治疗该病的有效药物，更好的为患者解除病痛，意义重大。本文主要通过以下几方面对该病进行研究。
综述一：中西医治疗DLASO研究进展
综述从中医辨证论治、专方专治、中药注射液治疗，中医外治疗法、现代医学治疗，中西医结合治疗及身心调护等方面归类总结了DLASO的治疗方法。
综述二：DLASO危险因素及发病机制的文献研究
综述分析归纳了年龄、性别、病程、吸烟、血糖、血压、血脂、血尿酸（UA）、纤维蛋白原(Fib)、CRP（CRP）等公认的DLASO相关危险因素的致病机理。
正文一：DLASO危险因素临床病例回顾性分析
目的：通过分析从2009年10月～2012年10月于我院内分泌科住院的4788例糖尿病患者的病例，对比其中部分病例的多项暴露因素及相关理化检查结果，明确引发DLASO的危险因素，为该病今后的临床防治及临床试验提供指导依据。
方法：检索及查阅近三年间4788例DM病例，结合临床症状、体征，经下肢动脉彩色多普勒超声检查确诊为DLASO者476例，选取其中资料相对完整的305例病例作为观察组，并从同期住院的无LASO的糖尿病患者（NDLASO）病例中随机抽取305例作为对照组。对两组病例进行回顾性对照分析，比较二者的年龄、糖尿病病程、吸烟史、饮酒史、体重指数（BMI）、收缩压（SBP）、舒张压（DBP）、空腹血糖（FPG）、餐后2小时的血糖（2hPG）、糖化血红蛋白(HbA1c)、甘油三酯（TG）、总胆固醇(CHOL)、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、UA、血肌酐（CREA）、血尿素（UREA）、CRP、双侧ABI数值等指标间差异，采用相应的统计学分析。并对DLASO组吸烟者与非吸烟者的CHOL、TG、HDL-C、LDL-C情况及女性与男性的患病年龄进行统计学比较。
结果：
1.自2009年10～2012年10月三年间，我院内分泌科DLASO患病率大于9.9%。
2.DLASO与NDLASO患者在年龄、糖尿病病程、吸烟史、BMI、SBP、DBP、UA、CREA、UREA、双侧ABI等方面进行比较，经秩和检验，P<0.05，差异有统计学意义，根据平均秩次结果，提示DLASO患者上述各项指标异常程度明显高于NDLASO的糖尿病患者。
3.DLASO组女性患病年龄明显高于男性，P<0.05，差异有统计学意义。
4.对两组患者的多种暴露因素和理化检查指标进行Logistic回归分析，其中年龄、病程、吸烟、UA、SBP进入回归方程,五项指标及相应偏回归检验的P值均<0.01，回归方程的准确率75.1%，具有统计学意义，方程成立。回归方程为：LogitP=-7.690+0.52年龄+0.128病程+0.593吸烟+0.002血尿酸+0.021收缩压。
结论：
1.本项研究发现，近三年于我院内分泌科住院的糖尿病患者中DLASO患病率约大于十分之一，表明本地区DLASO患者众多，且该类患者较NDLASO的糖尿病患者往往年龄更高、病程更长、BMI值更大、血压、UA、CREA、UREA也更高、并且具有明确的吸烟史者更多。因此建议NDLASO者减轻或保持体重适中、有效的控制血压、UA、CREA、UREA水平，戒烟并养成良好的生活习惯以延缓DLASO发生。
2.在诸多研究因素中，年龄,病程,吸烟, SBP, UA是DLASO发病的危险因素,其中吸烟、病程及年龄与DLASO的发生显著相关。
3.从性别角度，男性患DLASO的年龄往往早于女性。
正文二：木丹颗粒治疗糖尿病并下肢动脉硬化闭塞症临床研究
目的：木丹颗粒是于世家教授潜心多年研制而成的专门治疗糖尿病周围神经病变(DPN)的药物，已于2008年获国家药监局新药批产证书，其功效为益气活血，通络止痛。而DPN与DLASO的中医病机相似，且DLASO临床表现以肢体麻木凉痛为主，治疗亦重在活血化瘀，通络止痛。依据中医“异病同治”理论，推测木丹颗粒治疗DLASO也可能存在一定疗效，为进一步探讨木丹颗粒治疗DLASO之临床疗效，设计本项研究。
方法：将47例DLASO患者随机分为治疗组31例和对照组16例，两组在降糖、降压、调脂、抗血小板聚集、配合治疗仪局部治疗的基础上，治疗组口服木丹颗粒，对照组口服通塞脉片，两组均服药四周，四周后观察两组治疗前后临床证候积分及疗效，FPG、2hPG、TG、CHOL、HDL-C、LDL-C、全血黏度、毛细血管血浆粘度、红细胞压积、Fib、双下肢动脉内径及血流峰值速度的变化情况，然后进行相应的统计学处理。
结果：
1.木丹颗粒组总有效率为77.41%，通塞脉片组总有效率为68.75%,经X2检验，P>0.05，无统计学差异。
2.与各自治疗前相比两组治疗后TG、CHOL、HDL-C、LDL-C、FPG、2hPG、全血粘度、毛细血管血浆粘度、Fib、双侧胫前动脉及足背动脉的内径和血流峰值速度明显改善，P＜0.05，差异有统计学意义。
3.两组治疗后双侧胫后动脉内径及血流峰值速度比较，P<0.05,差异有统计学意义,但两组治疗前上述指标比较即存在统计学差异（P<0.05）,由此考虑两组治疗后的差异与治疗前即存在差异有关。
结论：
1.基础疗法配合木丹颗粒治疗气虚血瘀型DLASO临床疗效显著，总有效率可达77.41%，与治疗DLASO的专门药物通塞脉片疗效相当。
2.木丹颗粒可能通过调脂、降低全血粘度，溶解Fib、提高血流速度，扩张血管等途径有效改善下肢供血，从而达到治疗DLASO目的。
As one of the most common macroangiopathy, the incidence of diabetic lowerextremity arteriosclerosis obstruction (DLASO) is gradually increased in recentyears. The numb, cool, painful feeling of lower extremities sometimes can becomegangrene, and even be amputated, which make seriously negative impact on normalwork and life. So it's important to find the risk factors and effective medicineof DLASO, in order to prevent occurrence of the disease, and relieveindisposition from patients. As following there are four parts in our thesis.
First review: The research progress of DLASO on the treatmentof Traditional Chinese Medicine (TCM) and Western Medicine
This part is the literature review of Traditional Chinese Medicine (TCM),Western Medicine and integration of them, which is about the treatment of DLASO.It also contains the importance of regulating physical and mental health.
Second review: The research is about the risk factors andpathological mechanism of DLASO.
This part is a literature summary about the recognized risk factors of DLASO,such as age, sex, course of disease, smoking, blood glucose, blood pressure,lipids, UA, fibrinogen (Fib) and CRP as well as the pathological mechanism ofthem.
Text one: The retrospective study of clinical cases about DLASO.
Purpose: To find the risk factors, clinical treatment, guiding basis forclinical trials of DLASO, we analyzed and compared part of4788medical recordsof diabetes mellitus (DM) on multiple exposure factors and the results ofphysical and chemical examinations from2009to2012in our Department ofEndocrinology.
Methods: In4788patients there were476patients had been diagnosed as DLASOby color Doppler ultrasound. On the one hand we chose305medical records from 476records, which had comparatively complete informations, on the other hand305medical records were randomly selected from the4788patients of DM whohaven't LASO (NDLASO). We not only made contrast of parameters, which includingage, course of disease, history of smoking and drinking, BMI, SBP, DBP, FPG,2hPG, HbA1C, TG, CHOL, HDL-C, LDL-C, UA, CREA, UREA, CRP, the ABI of bilaterallimb, but also respectively compared the age and lipids of DLASO group throughsex and smoking history. The results were treated statistically.
Results:
1. The prevalence of DLASO was more than9.9%from2009to2012in our Departmentof Endocrinology.
2. The two groups had Statistically significant differences in aspects of age,course of disease, history of smoking，SBP, DBP, UA, CREA, UREA and the ABI ofbilateral limbs, through the analysis of wilcoxon rank sum test, which gave theresult of P<0.05. It also revealed that the condition of DLASO was worse thanthat of NDLASO depending on the mean rank.
3. P<0.05showed that there was remarkable difference in age between men andwomen of DLASO group. The average age of onset of women is elder than men.
4. Among multiple observed indexes, just age, course of disease, smoking, SBPand UA were selected into regression equation by way of Logistic regressionanalysis. The regression equation had Statistically significant with75.1%accuracy and test indicators,which is P<0.05.The equation was that: LogitP=-7.690+0.52age+0.128course+0.593smoke+0.002UA+0.021SBP.
Conclusion:
1. This study found that the prevalence of DLASO was nearly more than one tenthin our Department of Endocrinology from2009to2012.The digital indicated thatthere were plenty of DLASO patients in this region. To comparing with thepatients of NDLASO, people who had DLASO usually accompanied with older age,longer course of disease, higher value of BP, UA, BMI, CREA and UREA. They oftenhad history of smoking. In order to defer the happening of DLASO, we proposed that keeping effectively control of BP, UA, BMI, CREA as well as UREA and avoidingsmoking for NDLASO patients.
2. In variety of parameters, just age, course of disease, smoking, SBP, and UAwere statistically analyzed to be the risk factors of DLASO, especially the firstthree of them had remarkable relationship with DLASO.
3. The average age of women was elder than men in DLASO group, which indicatesthat gender differences had a significant impact on the occurrence of DLASO.
Text two： The clinical trial research about DLASO.
Purpose: As an effective Chinese patent medicine，which was developed fromProfessor Yu Shijia for diabetic peripheral neuropathy(DPN), Mudan granula(MDG)had obtained the batch production certificate from State Food and DrugAdministration（SFDA） in2008. It has the function of supplementing Qi,promoting blood circulation, dredging meridian and relieving pain.DLASO has thesimilar clinical manifestations and principles of treatment like DPN. Accordingto the theory of TCM, which indicates that treating different diseases with thesame method, we can infer that MDG may be has effect on the treatment of DLASO.So we designed this clinical trial in order to observe the efficacy of MDG forDLASO.
Methods:47patients were randomly assigned to the treatment group and thecontrol group. The former with31patients took MDG, while the latter with16patients took Tongsemai tablets(TSMT) on the basic therapy of hypoglycemic,hypotensive, regulating blood lipids, anti-platelet aggregation andtherapeutic apparatus. After four weeks, the integration and efficacy ofclinical symptom as well as the parameters were observed, which including FPG,2hPG, TG, CHOL, LDL-C, HDL-C, whole blood viscosity, plasma viscosity of bloodcapillary, hematocrit(HCT), fibrinogen(Fib), and blood dynamics of lower limbs．The results were treated statistically．
Results:
1. MDG group reaches the total efficiency as high as77.41%, while in TSMT groupthe total effective rate is68.75%. Chi-square(X2) analysis gives the result ofP>0．05，without significant difference．
2. After treatment, the statistical comparison of TG, CHOL, LDL-C, HDL-C, FPG,2hPG, whole blood viscosity, plasma viscosity of blood capillary, HCT, Fib, theinner diameter as well as peak velocity of blood flow of bilateral dorsalis pedisand anterior tibial artery between before and after treatment showed that P＜0.05, which had Statistically significant differences.
3. After treatment, P<0.05showed the significant differences between two groupsin the inner diameter and peak velocity of blood flow of bilateral posteriortibial artery, however we found that the diversity had already existed beforetherapy.
Conclusion:
1. MDG showed obvious efficacy in the treatment of DLASO with the syndrome ofQi deficiency and blood stasis on the basic therapy．MDG had similar efficacyas TSMT which is specially used on DLASO’s therapy.
2. The effective mechanism of MDG may not only contain regulating blood lipids，reducing whole blood viscosity, plasma viscosity of blood capillary, dissolvingFib, but also conclude accelerating blood flow and dilating blood vessels. Allof these are useful to reach the therapeutic purpose of improving the blood supplyof lower limbs．
综述一：中西医治疗DLASO研究进展
综述从中医辨证论治、专方专治、中药注射液治疗，中医外治疗法、现代医学治疗，中西医结合治疗及身心调护等方面归类总结了DLASO的治疗方法。
综述二：DLASO危险因素及发病机制的文献研究
综述分析归纳了年龄、性别、病程、吸烟、血糖、血压、血脂、血尿酸（UA）、纤维蛋白原(Fib)、CRP（CRP）等公认的DLASO相关危险因素的致病机理。
正文一：DLASO危险因素临床病例回顾性分析
目的：通过分析从2009年10月～2012年10月于我院内分泌科住院的4788例糖尿病患者的病例，对比其中部分病例的多项暴露因素及相关理化检查结果，明确引发DLASO的危险因素，为该病今后的临床防治及临床试验提供指导依据。
方法：检索及查阅近三年间4788例DM病例，结合临床症状、体征，经下肢动脉彩色多普勒超声检查确诊为DLASO者476例，选取其中资料相对完整的305例病例作为观察组，并从同期住院的无LASO的糖尿病患者（NDLASO）病例中随机抽取305例作为对照组。对两组病例进行回顾性对照分析，比较二者的年龄、糖尿病病程、吸烟史、饮酒史、体重指数（BMI）、收缩压（SBP）、舒张压（DBP）、空腹血糖（FPG）、餐后2小时的血糖（2hPG）、糖化血红蛋白(HbA1c)、甘油三酯（TG）、总胆固醇(CHOL)、高密度脂蛋白胆固醇（HDL-C）、低密度脂蛋白胆固醇（LDL-C）、UA、血肌酐（CREA）、血尿素（UREA）、CRP、双侧ABI数值等指标间差异，采用相应的统计学分析。并对DLASO组吸烟者与非吸烟者的CHOL、TG、HDL-C、LDL-C情况及女性与男性的患病年龄进行统计学比较。
结果：
1.自2009年10～2012年10月三年间，我院内分泌科DLASO患病率大于9.9%。
2.DLASO与NDLASO患者在年龄、糖尿病病程、吸烟史、BMI、SBP、DBP、UA、CREA、UREA、双侧ABI等方面进行比较，经秩和检验，P<0.05，差异有统计学意义，根据平均秩次结果，提示DLASO患者上述各项指标异常程度明显高于NDLASO的糖尿病患者。
3.DLASO组女性患病年龄明显高于男性，P<0.05，差异有统计学意义。
4.对两组患者的多种暴露因素和理化检查指标进行Logistic回归分析，其中年龄、病程、吸烟、UA、SBP进入回归方程,五项指标及相应偏回归检验的P值均<0.01，回归方程的准确率75.1%，具有统计学意义，方程成立。回归方程为：LogitP=-7.690+0.52年龄+0.128病程+0.593吸烟+0.002血尿酸+0.021收缩压。
结论：
1.本项研究发现，近三年于我院内分泌科住院的糖尿病患者中DLASO患病率约大于十分之一，表明本地区DLASO患者众多，且该类患者较NDLASO的糖尿病患者往往年龄更高、病程更长、BMI值更大、血压、UA、CREA、UREA也更高、并且具有明确的吸烟史者更多。因此建议NDLASO者减轻或保持体重适中、有效的控制血压、UA、CREA、UREA水平，戒烟并养成良好的生活习惯以延缓DLASO发生。
2.在诸多研究因素中，年龄,病程,吸烟, SBP, UA是DLASO发病的危险因素,其中吸烟、病程及年龄与DLASO的发生显著相关。
3.从性别角度，男性患DLASO的年龄往往早于女性。
正文二：木丹颗粒治疗糖尿病并下肢动脉硬化闭塞症临床研究
目的：木丹颗粒是于世家教授潜心多年研制而成的专门治疗糖尿病周围神经病变(DPN)的药物，已于2008年获国家药监局新药批产证书，其功效为益气活血，通络止痛。而DPN与DLASO的中医病机相似，且DLASO临床表现以肢体麻木凉痛为主，治疗亦重在活血化瘀，通络止痛。依据中医“异病同治”理论，推测木丹颗粒治疗DLASO也可能存在一定疗效，为进一步探讨木丹颗粒治疗DLASO之临床疗效，设计本项研究。
方法：将47例DLASO患者随机分为治疗组31例和对照组16例，两组在降糖、降压、调脂、抗血小板聚集、配合治疗仪局部治疗的基础上，治疗组口服木丹颗粒，对照组口服通塞脉片，两组均服药四周，四周后观察两组治疗前后临床证候积分及疗效，FPG、2hPG、TG、CHOL、HDL-C、LDL-C、全血黏度、毛细血管血浆粘度、红细胞压积、Fib、双下肢动脉内径及血流峰值速度的变化情况，然后进行相应的统计学处理。
结果：
1.木丹颗粒组总有效率为77.41%，通塞脉片组总有效率为68.75%,经X2检验，P>0.05，无统计学差异。
2.与各自治疗前相比两组治疗后TG、CHOL、HDL-C、LDL-C、FPG、2hPG、全血粘度、毛细血管血浆粘度、Fib、双侧胫前动脉及足背动脉的内径和血流峰值速度明显改善，P＜0.05，差异有统计学意义。
3.两组治疗后双侧胫后动脉内径及血流峰值速度比较，P<0.05,差异有统计学意义,但两组治疗前上述指标比较即存在统计学差异（P<0.05）,由此考虑两组治疗后的差异与治疗前即存在差异有关。
结论：
1.基础疗法配合木丹颗粒治疗气虚血瘀型DLASO临床疗效显著，总有效率可达77.41%，与治疗DLASO的专门药物通塞脉片疗效相当。
2.木丹颗粒可能通过调脂、降低全血粘度，溶解Fib、提高血流速度，扩张血管等途径有效改善下肢供血，从而达到治疗DLASO目的。
As one of the most common macroangiopathy, the incidence of diabetic lowerextremity arteriosclerosis obstruction (DLASO) is gradually increased in recentyears. The numb, cool, painful feeling of lower extremities sometimes can becomegangrene, and even be amputated, which make seriously negative impact on normalwork and life. So it's important to find the risk factors and effective medicineof DLASO, in order to prevent occurrence of the disease, and relieveindisposition from patients. As following there are four parts in our thesis.
First review: The research progress of DLASO on the treatmentof Traditional Chinese Medicine (TCM) and Western Medicine
This part is the literature review of Traditional Chinese Medicine (TCM),Western Medicine and integration of them, which is about the treatment of DLASO.It also contains the importance of regulating physical and mental health.
Second review: The research is about the risk factors andpathological mechanism of DLASO.
This part is a literature summary about the recognized risk factors of DLASO,such as age, sex, course of disease, smoking, blood glucose, blood pressure,lipids, UA, fibrinogen (Fib) and CRP as well as the pathological mechanism ofthem.
Text one: The retrospective study of clinical cases about DLASO.
Purpose: To find the risk factors, clinical treatment, guiding basis forclinical trials of DLASO, we analyzed and compared part of4788medical recordsof diabetes mellitus (DM) on multiple exposure factors and the results ofphysical and chemical examinations from2009to2012in our Department ofEndocrinology.
Methods: In4788patients there were476patients had been diagnosed as DLASOby color Doppler ultrasound. On the one hand we chose305medical records from 476records, which had comparatively complete informations, on the other hand305medical records were randomly selected from the4788patients of DM whohaven't LASO (NDLASO). We not only made contrast of parameters, which includingage, course of disease, history of smoking and drinking, BMI, SBP, DBP, FPG,2hPG, HbA1C, TG, CHOL, HDL-C, LDL-C, UA, CREA, UREA, CRP, the ABI of bilaterallimb, but also respectively compared the age and lipids of DLASO group throughsex and smoking history. The results were treated statistically.
Results:
1. The prevalence of DLASO was more than9.9%from2009to2012in our Departmentof Endocrinology.
2. The two groups had Statistically significant differences in aspects of age,course of disease, history of smoking，SBP, DBP, UA, CREA, UREA and the ABI ofbilateral limbs, through the analysis of wilcoxon rank sum test, which gave theresult of P<0.05. It also revealed that the condition of DLASO was worse thanthat of NDLASO depending on the mean rank.
3. P<0.05showed that there was remarkable difference in age between men andwomen of DLASO group. The average age of onset of women is elder than men.
4. Among multiple observed indexes, just age, course of disease, smoking, SBPand UA were selected into regression equation by way of Logistic regressionanalysis. The regression equation had Statistically significant with75.1%accuracy and test indicators,which is P<0.05.The equation was that: LogitP=-7.690+0.52age+0.128course+0.593smoke+0.002UA+0.021SBP.
Conclusion:
1. This study found that the prevalence of DLASO was nearly more than one tenthin our Department of Endocrinology from2009to2012.The digital indicated thatthere were plenty of DLASO patients in this region. To comparing with thepatients of NDLASO, people who had DLASO usually accompanied with older age,longer course of disease, higher value of BP, UA, BMI, CREA and UREA. They oftenhad history of smoking. In order to defer the happening of DLASO, we proposed that keeping effectively control of BP, UA, BMI, CREA as well as UREA and avoidingsmoking for NDLASO patients.
2. In variety of parameters, just age, course of disease, smoking, SBP, and UAwere statistically analyzed to be the risk factors of DLASO, especially the firstthree of them had remarkable relationship with DLASO.
3. The average age of women was elder than men in DLASO group, which indicatesthat gender differences had a significant impact on the occurrence of DLASO.
Text two： The clinical trial research about DLASO.
Purpose: As an effective Chinese patent medicine，which was developed fromProfessor Yu Shijia for diabetic peripheral neuropathy(DPN), Mudan granula(MDG)had obtained the batch production certificate from State Food and DrugAdministration（SFDA） in2008. It has the function of supplementing Qi,promoting blood circulation, dredging meridian and relieving pain.DLASO has thesimilar clinical manifestations and principles of treatment like DPN. Accordingto the theory of TCM, which indicates that treating different diseases with thesame method, we can infer that MDG may be has effect on the treatment of DLASO.So we designed this clinical trial in order to observe the efficacy of MDG forDLASO.
Methods:47patients were randomly assigned to the treatment group and thecontrol group. The former with31patients took MDG, while the latter with16patients took Tongsemai tablets(TSMT) on the basic therapy of hypoglycemic,hypotensive, regulating blood lipids, anti-platelet aggregation andtherapeutic apparatus. After four weeks, the integration and efficacy ofclinical symptom as well as the parameters were observed, which including FPG,2hPG, TG, CHOL, LDL-C, HDL-C, whole blood viscosity, plasma viscosity of bloodcapillary, hematocrit(HCT), fibrinogen(Fib), and blood dynamics of lower limbs．The results were treated statistically．
Results:
1. MDG group reaches the total efficiency as high as77.41%, while in TSMT groupthe total effective rate is68.75%. Chi-square(X2) analysis gives the result ofP>0．05，without significant difference．
2. After treatment, the statistical comparison of TG, CHOL, LDL-C, HDL-C, FPG,2hPG, whole blood viscosity, plasma viscosity of blood capillary, HCT, Fib, theinner diameter as well as peak velocity of blood flow of bilateral dorsalis pedisand anterior tibial artery between before and after treatment showed that P＜0.05, which had Statistically significant differences.
3. After treatment, P<0.05showed the significant differences between two groupsin the inner diameter and peak velocity of blood flow of bilateral posteriortibial artery, however we found that the diversity had already existed beforetherapy.
Conclusion:
1. MDG showed obvious efficacy in the treatment of DLASO with the syndrome ofQi deficiency and blood stasis on the basic therapy．MDG had similar efficacyas TSMT which is specially used on DLASO’s therapy.
2. The effective mechanism of MDG may not only contain regulating blood lipids，reducing whole blood viscosity, plasma viscosity of blood capillary, dissolvingFib, but also conclude accelerating blood flow and dilating blood vessels. Allof these are useful to reach the therapeutic purpose of improving the blood supplyof lower limbs．
引文
[1]秦红松，陈柏楠.德俊教授从整体与局部相结合论治闭塞性动脉硬化症经验.山东中医药大学学报,2006,30(30):206-208.
[2]李振中，尹翠梅，丁学屏.再论痰浊与糖尿病血管病变.江西中医药，2005，4(4)，36(268):15.
[3]陈淑长．中医血管外科学.中国医药科技出版社，1993年7月第l版，176-177.
[4]刘孟安，徐金元，姜学连.补阳还五汤对糖尿病闭塞性动脉硬化症的临床研究.中国医药学报，1998，13(6):21-22.
[5]马锐，赵建宛.温阳通脉汤治疗糖尿病下肢动脉硬化闭塞症120例[J].中医临床研究，2011，3（6）：13-14.
[6]李德海，余武，蔡莉莉,等.三七通舒治疗糖尿病合并下肢动脉硬化的疗效观察[J].湖北中医杂志，2007，29（5）：38-39.
[7]任志雄.糖痛方治疗早期糖尿病性动脉闭塞症的临床研究：（博士学位论文）.北京：北京中医药大学，2004.
[8]徐灿坤,曲竹秋.翻地还五汤治疗糖尿病肢体动脉闭塞症疗效观察.辽宁中医杂志，2006，33（7）：835.
[9]韩建勤,张彦宁,赵通洲,等.雷公藤治疗糖尿病下肢动脉硬化闭塞症.实用糖尿病杂志，2007，3（1）：50-51.
[10]苏立德,颜纪贤.雷化藤多甙治疗系统性硬皮病临床观察.中国中西医结合杂志，1994,4:234-235.
[11]陈星,丰美富,朱国英.雷公藤红素对血管平滑肌细胞内游离Ca2+和H+浓度的影响[J].中国中西医结合杂志,1999,19(9):538-540.
[12]刘志伟.丹红注射液治疗2型糖尿病下肢AS闭塞症68例疗效观察[J].山东中医，2007，47（28）107-108.
[13]刘艳，郭晖，杨松青,等.刺五加治疗糖尿病下肢动脉硬化闭塞症44例.吉林大学学报（医学版）,2003，29（6）：821-823.
[14]季守贤,包红.刺五加治疗糖尿病性脑梗塞疗效分析[J].中风与神经疾病杂志,1997,14(4):241.
[15]郭水英.大剂量刺五加注射液治疗周围血管病的血液流变学观察[J].实用中西医结合杂志,1993,(2):114-115.
[16]刘玉兰,王世久,蔡玉珉.刺五加茎叶对血小板聚集功能的影响[J].沈阳药学院学报,1989,6(1):57-60.
[17] Johnson GJ, Dunlop PC, Leis LA, et al. Dihydropyridine agonist Bay K8644inhibits platelet activation by competitive antagonism of thromboxaneA2-prostaglandin H2receptor. Circ Res,1988,62(3):494-505.
[18]王树立,李永德,赵勤,等.山楂、黄芪、刺五加对豚鼠胆固醇代谢的影响初报[J].河南医学情报,1987,4(8):783-785.
[19]倪劲松,吴家祥,肖幻秋,等.刺五加皂甙对糖尿病大鼠血过氧化脂质和超氧化物歧化酶的影响[J].白求恩医科大学学报,1998,24(1):33-34.
[20]罗礼东.灯盏花素注射液治疗下肢动脉硬化闭塞症38例临床观察.福建医药杂志，2005,27(6):153-154.
[21]王影,杨祥良,刘宏，等.灯盏花素抗凝作用的研究.中药材,2003,26(9):656-658.
[22]张颖,李玲妹,孙京晶,等.注射用灯盏花素治疗缺血性脑血管病43例临床观察.中华临床医药,2003,4(5):9.
[23]冯琨,谭静范,陈影,等.疏血通注射液治疗糖尿病下肢动脉硬化闭塞症临床观察.中国中西医结合杂志，2009,29(3):255-256.
[24]刘皓,崔炎,刘辉,等.中药外治糖尿病肢体动脉闭塞症.中国中西医结合外科杂志.2009,25(3):271-272.
[25]任文英,李建民,赵丹阳,等.中药外洗联合前列腺E1(PGE1)治疗糖尿病下肢动脉硬化闭塞症48例.陕西中医学院学报，2008，31（1）：35-36.
[26]郝威威.糖尿病并下肢动脉硬化闭塞症益气活血中药促进干细胞移植后血管分化的试验研究，2007，5：1-45.
[27]何晓兰.益气通脉方合外洗方治疗早期糖尿病下肢动脉硬化闭塞症的临床观察.北京中医.2005，24(4):195-196.
[28]焦海强，孙传聪.动静脉泵LBTK-M-I1000在下肢动脉硬化症患者中的应用.现代诊断与治疗，2012,23(7):985-986.
[29]刘洪涛,祖茂衡,徐浩,等.讨微波深部热疗治疗老年下肢动脉硬化闭塞症.中外医疗（临床医学），2010,31:91.
[30]赵钢,吕勃川,于文慧.巴曲酶和前列地尔治疗下肢动脉硬化闭塞症193例.中国中西医结合外科杂志，2009,15(1):45-46.
[31]李昌祁,冯佳庆,黄晓玲，等.东菱迪芙治疗糖尿病周围血管病变多项目观察附32例临床分析[J].中国医药指南,2007,5(9):38.
[32]华智强,王滨.东菱迪芙治疗糖尿病周围神经病变60例疗效观察[J].中国实用神经疾病杂志，2006,9(6):133.
[33] Kernick DP, Shore AC. Characteristics of laser Doppler perfusion imagingin vitro and in vivo. Physiol Meas,2000,21(2):333-340.
[34]姜宗,曹丽英.前列地尔在临床上的应用[J].中国老年学杂志,2003,9(23):628.
[35]莫励敏.中西医结合治疗糖尿病并下肢动脉硬化60例.中国民间疗法，2007，13（9）：6-7.
[36]丁学屏.中西医结合糖尿病学.北京:人民卫生出版社,2004年3月第1版，35-425.
[37]刘汉庆.中西医结合治疗糖尿病肢体动脉硬化性闭塞症35例.安徽中医学院学报.2009,28(1):21.
[38]姜凯,黄丽秋,高凯,等.中西医结合治疗下肢动脉硬化闭塞症47例.长春中医药大学学报，2009，25（1）：103-105.
[39]兰静.辨证施护对LASO的影响.中国中医急症，2010,19(6):1073-1074.
[1]潘长玉，高妍，袁申元，等，2型糖尿病下肢血管病变发生率及相关因索调查[J].中国糖尿病杂志，2001，5(9):323.
[2]谢铮伟.补阳还五汤加味对糖尿病闭塞性动脉硬化症的临床观察.安徽卫生职业技术学院学报，2004，3(2):21-12.
[3]张亿倬,韩继武,黄玉玲.动脉硬化超声所见与危险因子及年龄的相关性[J].中国临床康复,2005,9(41):34-36.
[4] Taddei S, Virdis A, Mattei P, et al. Aging and endothelial function innormotensive subjects and patients with essential hypertension. Circulation,1995,91（7）:1981-1987.
[5] Vander meer IM, Iglesias del Sol A, Wittenman JC, et al. Risk factors forprogression of atherosclerosis measured at multiple sites in the arterial tree:the Rotterdam Study. Stroke,2003,34(10):2374-2379.
[6]邱飞.肿瘤坏子因子α与心力衰竭的研究进展.国外医学·药学分册.2003,30(6):326-330.
[7]李小鹰，范利。老年周围动脉硬化闭塞性疾病[M]．济南：山东科学技术出版社，2003年8月第1版，1-142.
[8]胡承恒，杜志民，罗初凡，等．年龄与性别在冠状动脉钙化程度和冠心病的诊断价值中的影响[J]．中华心血管病杂志，2001，29（11）：668-671.
[9] Grodstein F，Stampfer MJ，Cobditz GA，et a1．Postmenopausal Hormone Therapyand Mortality. N Engl J Med，1997，337(19)：1389-1391.
[10]阮云军，吴赛珠，孟素荣，等.雌激素对血管内皮细胞一氧化氮合成酶活性调控的受体机制研究.中华老年心脑血管病杂志，2000,2(4):263-265.
[11]染春卉，梁伯平，张晶.绝经期女性雌激素水平与血脂关系分析.临床心血管病杂志，1999,15(5)：232.
[12]叶文翔编著.脑血管疾病.北京：中国医药科技出版社,1990年3月第1版,110.
[13]陈兴洲译.吸烟是卒中的危险因素.国外医学脑血管疾病分册，1995，3(3):122.
[14]马温良,王艳,陈荣杰，等.吸烟与动脉硬化性脑梗塞关系的研究[J].中国慢性病预防与控制，1999,7(3):101.
[15]赵忠信，王彦华.血液高凝状态的相关因素[J].现代诊断与治疗，1998,9(6):381-382.
[16] Jackson WF. Quick change artist: endothelium-derived relaxing factor inresistance arteries. Hypertansion,2011,57(4):686-688.
[17]邓发达，戴亚，朱立军，等.卷烟烟气中一氧化氮研究进展.烟草科技／烟草化学，2004,11(208):24.
[18]张育，郑诚东，张代民，等.吸烟对健康人血清HDL-C等7项指标水平影响的对比观察[J].中华流行病学杂志，1992,13（2）：97.
[19] Wallis WJ, Beatty PG, Ochs HD, et al. Human monocyte adherence to culturedvascular endothelium: monoclonal antibody-defined mechanisms. J Immunol,1985,135(4):2323-2330.
[20] Willett W, Hennekens CH, Castelli W, et al. Effects of cigarette smokingon fasting triglyceride, total cholesterol, and HDL-cholesterol in women. AmHeart J,1983,105(3):417-421.
[21]毕小云，邓小玲，肖琴，等.吸烟对血脂的影响[J].重庆医科大学学报，2004,29(1):80-82.
[22] Kong C，Nimmo L，Elatrozy T, et al. Smoking is associated with increasedhepatic lipase activity, insulin resistance, dyslipidaemia and earlyatherosclerosis in Type2diabetes. Atherosclerosis,2001,156(2):373-378.
[23]念馨,张旭祥,宋滇平.2型糖尿病下肢血管病变相关因素分析.中华临床医师杂志，2007,1(5):33-34.
[24]赵水平．临床血脂学[M]．北京：人民卫生出版社，2006年12月第1版，11-234.
[25] Piantadosi CA, Schwartz DA. The acute respiratory distress syndrome. AnnIntern Med,2004,141(6):460-470.
[26] Puneet P, Moochhala S, Bhatia M. Chemokines in acute respiratory distresssyndrome. Am J Physiol Lung Cell Mol Physiol,2005,288(1):L3-L15.
[27]刘莉，叶鹏.SBP变异性与2型糖尿病患者糖尿病肾病及动脉粥样硬化相关.中华高血压杂志，2012，6（20）:599-560.
[28]刘燕.2型糖尿病合并高血压LASO危险因素分析[J].现代诊断与治疗，2012,23(6):841.
[29]侯德凤.血脂和载脂蛋白ApoA1、ApoB的测量与糖尿病合并血管病变的关系［J］.华夏医学，2000，13（3）：360.
[30]马绍杰，王颖，金秀平.2型糖尿病大血管病变相关因素分析.华北煤炭医学院学报，2004,6(4):446-447.
[31]赵水平.糖尿病血脂异常及治疗.中华内科杂志,2002,41(5):356-358.
[32]黄峻，刘超，丁国宪．代谢综合征与心血管疾病[M]．北京：科学出版社，2004年5月第1版，232-236.
[33]洪华山,刘翼,王一波,等.糖基化低密度脂蛋白增加血管内皮对单核细胞的粘附作用.中华内分泌代谢杂志,1998,4(14):48-50.
[34]刘秉文，曾成林.高密度脂蛋白抗AS作用[J],中国动脉硬化志，1994,2(1):45-47.
[35] Fernandez ML, McNamara DG. High-density lipoprotein binding to guinea-pighepatic membranes. Comparison of guinea-pig and human ligands. Biochim BiophysActa,1990，1042(1):142-145.
[36] Brinton EA, Oram JF, Chen CH, et a1．Binding of high density lipoproteinto cultured fibroblasts after chemical alteration of apoprotein amino acidresidues. J Biol Chem,1986，261(1)：495-503.
[37] Chajek T, Aron L, Fielding CJ．Interaction of lecithin: cholesterolacyltransferase and cholesteryl ester transfer protein in the transport ofcholesteryl ester into sphingomyelin liposomes. Biochemistry,1980,19(16)：3673-3677.
[38] Shastri KM, Carvalho AC, Lees RS, et a1．Platelet function and plateletlipid composition in the dyslipoproteinemias. Lipid Res，1980，21(4):467-472.
[39]王锦淳.黄芩茎叶总黄酮对高甘油三酯诱导的血管内皮细胞氧化损伤的保护作用及机制研究.扬州大学学报，2012,38(3):397-340.
[40] Keaney JF Jr. Oxidative stress and the vascular wall: NADPH oxidases takecenter stage. Circulation,2005,112(17):2585-2588.
[41]廖志红，余斌杰．2型糖尿病血脂代谢紊乱及其控制[J]．中华内分泌杂志，2002，14(4)：277．
[42] Jandeleit-Dahm K, Cooper ME. The role of AGEs in cardiovascular disease.Curr Pharm Des,2008,14(10):979-986.
[43] Duh E, Aiello LP. Vascular endothelial growth factor and diabetes: theagonist versus antagonist paradox. Diabetes,1999,48(10):1899-1906.
[44] Shoji T, Koyama H, Morioka T, et al. Receptor for advanced glycation endproducts is involved in impaired angiogenic response in diabetes. Diabetes,2006,55(8):2245-2255.
[45] Renard C, Chappey O, Wautier MP, et al. Recombinant advanced glycation endproduct receptor pharmacokinetics in normal and diabetic rats.. Mol Pharmacol,1997,52(1):54-62.
[46] Wautier MP, Chappey O, Corda S, et al. Activation of NADPH oxidase by AGElinks oxidant stress to altered gene expression via RAGE. Am J Physiol EndocrinolMetab,2001,280(5): E685-E694.
[47] Ahmad FK, He Z, King GL. Molecular targets of diabetic cardiovascularcomplications. Curr Drug Targets,2005,6(4):487-494.
[48] Hammes HP. Pathophysiological mechanisms of diabetic angiopathy. J DiabetesComplications,2003,17(2Suppl):16-19.
[49] Anderson HD, Rahmutula D, Gardner DG. Tumor necrosis factor-alpha inhibitsendothelial nitric-oxide synthase gene promoter activity in bovine aorticendothelial cells. J Biol Chem,2004,279(2):963-969.
[50] Evans JL, Goldfine ID, Maddux BA, et al. Are oxidative stress-activatedsignaling pathways mediators of insulin resistance and beta-cell dysfunction?Diabetes,2003,52(1):1-8.
[53] Johansen JS, Harris AK, Rychly DJ, et al. Oxidative stress and the use ofantioxidants in diabetes: linking basic science to clinical practice. CardiovascDiabetol,2005,4(1):5.
[51] Maritim AC, Sanders RA, Watkins JB3rd. Diabetes, oxidative stress, andantioxidants: a review. J Biochem Mol Toxicol,2003,17(1):24-38.
[52] Patterson RA, Horsley ET, Leake DS. Prooxidant and antioxidant propertiesof human serum ultrafiltrates toward LDL: important role of uric acid. J LipidRes,2003,44(3):512-521.
[53] Sanguinetti SM, Batthyany C, Trostchansky A, et al. Nitric oxide inhibitsprooxidant actions of uric acid during copper-mediated LDL oxidation.. ArchBiochem Biophys,2004,423(2):302-308.
[54]孙海鸥.尿酸与AS关系的基础与临床初步研究：（硕士研究生毕业论文），第四军医大学.
[55] Nakagawa T, Zharikov S, Tuttle KR, et al. A causal role for uric acid infructose-induced metabolic syndrome. Am J Physiol Renal Physiol,2006,290(3):F625-631.
[56] Kanellis J, Kang DH. Uric acid as a mediator of endothelial dysfunction,inflammation and vascular disease.Semin Nephrol,2005,25(1):39-42.
[57] Leyva F, Anker S, Swan JW et al. Serum uric acid as an index of impairedoxidative metabolism in chronic heart failure. Eur Heart J,1997,18(5):858-865.
[58]张福琴，李志超，赵德,等.5-羟色胺在野百合碱引起大鼠肺动脉高压发病中的作用.中国病理生理杂志,1999,15（5）:462-466.
[59]彭荔薰，冯波. NIDDM患者血浆组织型纤维蛋白溶酶原激活物及其抑制物活性水平与胰岛素抵抗的探讨.中华内分泌代谢杂志,1995.2(3):110-112.
[60] Kawamoto R, Tomita H, Oka Y, et al. Association between uric acid and carotidatherosclerosis in elderly persons. Intern Med,2005,44(8):787-793.
[61]余振球，赵连友，刘国杖.高血压防治进展与实践［M］.北京:科学出版社，2003年1月第1版，254.
[62]张敏.Ⅱ型糖尿病患者血尿酸水平与血管并发症的相关性研究.中国实用医药，2011，6（14）:1131-1134.
[63]宫国东，宁为民，林家东.高尿酸血症与动脉硬化性脑梗死的关系研究.吉林医学，2010,31（24）：4065.
[64] Farquharson CA, Butler R, Hill A, et al. Allopurinol improves endothelialdysfunction in chronic heart failure. Circulation,2002,106(2):221-226.
[65] Doehner W, Schoene N, Rauchhaus M, et al. Effects of xanthine oxidaseinhibition with allopurinol on endothelial function and peripheral blood flowin hyperuricemic patients with chronic heart failure: results from2placebo-controlled studies. Circulation,2002,105(22):2619-2624.
[66]王雪青，刘乃奎，董林旺，等．纤维蛋白原在AS中的作用[J]．中国病理生理杂志，1997，3(3)：270-273.
[67] Sato S，Nakamura N，Iida M，et a1．Plasma fibrinogen and coronary heartdisease in urban Japanese. Am J Epidemiol，2000，152(5)：420-423.
[68] Loukas M，Dabrowski M，Wagner T，et a1．Fibrinogen and smooth muscle celldetection in atherosclerotic plaques from stable and unstable angina-animmunohistochemical study．Med Sci Monit，2002，8(4):BR144-148.
[69] Fibrinogen Studies Collaboration．Danesh J, Lewington S, Thompton SG, etal. Plasma fibrinogen level and the risk of major cardiovascular diseases andnonvascular mortality: an individual participant meta-analysis．JAMA，2005，294(14)：1799-1809.
[70]王洁，李小鹰，何耀，等．老年周围动脉硬化闭塞病与血浆纤维蛋白原、血小板集聚率关系的研究[J]．中华流行病学杂志，2005，26(1)：l-4.
[71]李丽,高大胜.血浆纤维蛋白原与冠状AS性心脏病的相关性研究[J].实用全科医学,2008,6(3):228-229.
[72] Lind P, Hedblad B, Stavenow L, et al. Influence of plasma fibrinogen levelson the incidence of myocardial infarction and death is modified by otherinflammation-sensitive proteins: a long-term cohort study.. Arterioscler ThrombVasc Biol,2001,21(3):452-458.
[73] Mortensen RF, Zhong W. Regulation of phagocytic leukocyte activities byC-reactive protein. J Leukoc Biol,2000,67(4):495-500.
[74] Zhang YX, Cliff WJ, Schoefl GI, et al. Coronary C-reactive proteindistribution: its relation to development of atherosclerosis.. Atherosclerosis,1999,145(2):375-379.
[75] Verma S, Wang CH, Li SH, et al. A self-fulfilling prophecy: C-reactiveprotein attenuates nitric oxide production and inhibits angiogenesis.Circulation,2002,106(8):913-919.
[76] Torzewski J. C-reactive protein and atherogenesis: new insights fromestablished animal models. Am J Pathol,2005,167(4):923-925.
[77] Zwaka TP, Hombach V, Torzewski J. C-reactive protein-mediated low densitylipoprotein uptake by macrophages: implications for atherosclerosis. Cirulation,2001,103(9):1194-1197.
[78]潘清蓉,孙梅励. C反应蛋白在AS中的作用[J].基础医学与临床,2004,24(4):462-465.
[79] Wang CH, Li SH, Weisel RD, et al. C-reactive protein upregulates angiotensintype1receptors in vascular smooth muscle[J]. Circulation,2003,107(13):1783-1790.
[80] Devaraj S, Xu DY, Jialal I, et al. C-reactive protein increases plasminogenactivator inhibitor-1expression and activity in human aortic endothelial cells:implications for the metabolic syndrome and atherothrombosis[J].Circulation,2003,107(3):398-404.
[1]杨文英等.中国2型糖尿病防治指南.北京：北京大学医学出版社.2011年9月第1版，3-50.
[2]张亿倬,韩继武,黄玉玲.动脉硬化超声所见与危险因子及年龄的相关性[J].中国临床康复,2005,9(41):34-36.
[3] Taddei S, Virdis A, Mattei P, et al. Aging and endothelial function innormotensive subjects and patients with essential hypertension. Circulation,1995,91(7):1981-1987.
[4] Vander meer IM, Iglesias del Sol A, Wittenman JC, et al. Risk factorsfor progression of atherosclerosis measure at multiple sites in the arterialtree: the Rotterdam Study.Stroke,2003,34(10):2374-2379.
[5]邱飞.肿瘤坏子因子α与心力衰竭的研究进展.国外医学·药学分册，2003,30(6):326-330.
[6] Asakawa H, Toktmaga K, Kawakami F. Comparison of risk factors ofmacrovascular comp lications peripheral vascular disease, cembral vasculardisease, and coronary heart dlsease in Japanes type2diabetes mellitus patients.J Diabetes Comp,2000,14(4):307-313.
[7]念馨,张旭祥,宋滇平.2型糖尿病下肢血管病变相关因素分析.中华临床医师杂志，2007,1(5):33-34.
[8] Piantadosi CA, Schwartz DA. The acute respiratory distress syndrome. AnnIntern Med,2004,141(6):460-470.
[9] Puneet P, Moochhala S, Bhatia M, Chemokines in acute respiratory distresssyndrome. Am J Physiol Lung Cell Mol Physiol,2005,288(1):L3-L5.
[10]刘莉，叶鹏.SBP变异性与2型糖尿病患者糖尿病肾病及AS相关.中华高血压杂志，2012，6（3）：65-67.
[11]刘燕.2型糖尿病合并高血压LASO危险因素分析[J].现代诊断与治疗，2012,23(6):841.
[12] Levenson JA, Simon AC, Safar ME, et al. Systolic hypertension inarteriosclerosis obliterans of the lower limbs. Clin Exp Hypertens A,1982,4(7):1059-1072.
[13] Nakagawa T, Zharikov S, Hu H, et al. A causal role for uric acid infructose-induced metabolic syndrome. Am J Physiol Renal Physiol,2006,290(3):F625-F631.
[14] Kanellis J, Kang DH. Uric acid as a mediator of endothelial dysfunction,inflammation and vascular disease. Semin Nephrol,2005,25(1):39-42.
[15] Leyva F, Anker S, Swan JW, et al. Serum uric acid as an index of impairedoxidative metabolism in chronic heart failure.. Eur Heart J,1997,18(5):858-865.
[16]张福琴，李志超，赵德，等.5-羟色胺在野百合碱引起大鼠肺动脉高压发病中的作用.中国病理生理杂志,1999，5（15）：1120-1123.
[17]彭荔薰，冯波. NIDDM患者血浆组织型纤维蛋白溶酶原激活物及其抑制物活性水平与胰岛素抵抗的探讨.中华内分泌代谢杂志,1995.2（4）：110-112.
[18] Kawamoto R, Tomita H, Oka Y. Association between uric acid and carotidatherosclerosis in elderly persons.Intern Med,2005,44(8):787-793.
[19]余振球，赵连友，刘国杖.高血压防治进展与实践［M］.北京:科学出版社，2003年1月第1版，254.
[20]张敏.Ⅱ型糖尿病患者血尿酸水平与血管并发症的相关性研究.中国实用医药，2011，6（14）：1131-1134.
[21]宫国东，宁为民，林家东.高尿酸血症与动脉硬化性脑梗死的关系研究.吉林医学，2010，31（24）：4065.
[22] Farquharson CA, Butler R, Hill A, et al. Allopurinol improves endothelialdysfunction in chronic heart failure.. Circulation,2002,106(2):221-226.
[23] Doehner W, Schoene N, Rauchhaus M, et al. Effects of xanthine oxidaseinhibition with allopurionl on endothelail function and peripheral blood flowin hyperuricemic patients with chronic heart failure: results from2placebo-controlled studies. Circulation,2002,105(22):2619-2624.
[24]叶文翔编著.脑血管疾病.北京：中国医药科技出版社,1990年3月第1版,110.
[25]陈兴洲译.吸烟是卒中的危险因素.国外医学脑血管疾病分册，1995，3(3):122.
[26]马温良,王艳,陈荣杰，等.吸烟与动脉硬化性脑梗塞关系的研究[J].中国慢性病预防与控制.1999,7(3):101.
[27]赵忠信，王彦华.血液高凝状态的相关因素[J].现代诊断与治疗，1998,9(6):381-382.
[28] Jackson WF. Quick change artist: endothelium-derived relaxing factor inresistance arteries. Hypertension,2011,57(4):686-688.
[29]邓发达，戴亚，朱立军，等.卷烟烟气中一氧化氮研究进展.烟草科技／烟草化学，2004,11(208):24.
[30]张育，郑诚东，张代民，等.吸烟对健康人血清HDL-C等7项指标水平影响的对比观察[J].中华流行病学杂志，1992,13（2）：97.
[31] Wallis WJ, Beatty PG, Ochs HD, et al. Human monocyte adherence to culturedvascular endothelium: monoclonal antibody-defined mechanisms. J Immunol,1985,135(4):2323-2330.
[32] Willett W, Hennekens CH, Castelli W, et al. Effects of cigarette smokingon fasting triglyceride, total cholesterol, and HDL-cholesterol in women. AmHeart J,1983,105(3):417-421.
[33]毕小云，邓小玲，肖琴等.吸烟对血脂的影响[J].重庆医科大学学报，2004,29(1):80-82.
[34] Kong C，Nimmo L，Elatrozy T, et al. Smoking is associated with increasedhepatic lipase activity, insulin resistance, dyslipidaemia and earlyatherosclerosis in Type2diabetes. Atheroclerosis,2001,156(2):373-378.
[35]刘秉文，曾成林.高密度脂蛋白抗AS作用[J].中国动脉硬化志，1994,2(1):45-47.
[36] Fernandez ML, McNamara DG. High-density lipoprotein binding to guinea-pighepatic membranes. Comparison of guinea-pig and human ligands. Biochim BiophysActa,1990，1042(1):142-145.
[37] Brinton EA, Oram JF, Chen CH, et a1．Binding of high density lipoproteinto cultured fibroblasts after chemical alteration of apoprotein amino acidresidues. J Biol Chem,1986，261(1)：495-503.
[38] Chajek T, Aron L, Fielding CJ．Interaction of lecithin: cholesterolacyltransferase and cholesteryl ester transfer protein in the transport ofcholesteryl ester into sphingomyelin liposomes. Biochemistry,1980,19(16)：3673-3677.
[39] Shastri KM, Carvalho AC, Lees RS, et a1．Platelet function and plateletlipid composition in the dyslipoproteinemias. Lipid Res，1980，21(4):467-472.
[1]潘长玉，高妍，袁申元，等，2型糖尿病下肢血管病变发生率及相关因索调查[J].中国糖尿病杂志，2001,(9)：323.
[2]中国中西医结合学会周围血管疾病专业委员会.糖尿病肢体动脉闭塞症诊断及疗效标准(草案).中西医结合心脑血管病杂志，2004(6)，2(6):352.
[3]陈淑长，葛苋主编．周围血管病的研究进展与中医治疗经验．北京：学苑出版社，2002年1月第1版，259-260.
[4]高雪敏主编.中药学.北京：中国中医药出版社，2002年9月第1版，364-366.
[5]雷载权主编.中药学.上海：上海科学技术出版社出版.1998年6月第1版，307-308.
[6]崔艳君，陈若芸.鸡血藤化学和药理研究进展.天然产物研究与开发，2006，15(4):72.
[7]仇锦春，卞慧敏.通塞脉片对大鼠实验性高脂血症及AS的影响[J].上海中医药杂志，2007，41（1）：71-73.
[8]顾锡镇.通塞脉片治疗急性脑缺血性中风30例.南京中医药大学学报，2004，20（2）：831.
[9]杨军，屈立志.通塞脉片对深静脉血栓形成纤溶功能的实验观察[J].中药新药与临床药理，2003，4（1）：32-33.
[10]姜淼，卞慧敏.通塞脉片对AS模型大鼠的影响[J].新中医，2007，39（12）：102-104.
[11]徐婷，王微.牛膝水煎液对自发性高血压大鼠血压和左心室肥厚的影响[J].长春中医药大学学报，2008，24（4）：367-368.
[12] Chen H, Li D, Sawamura T, et al. Upregulation of LOX-1expression in aortaof hypercholesterolemic rabbits: modulation by losartan. Biochem Biophys ResCommon,2000,276(3):1100-1104.
[13]李敏，孙虹，李琰.不同产地当归对血小板聚集及凝血时间活性的比较.中国中医基础医学杂志，2003，9（2）：47-50.
[2]李振中，尹翠梅，丁学屏.再论痰浊与糖尿病血管病变.江西中医药，2005，4(4)，36(268):15.
[3]陈淑长．中医血管外科学.中国医药科技出版社，1993年7月第l版，176-177.
[4]刘孟安，徐金元，姜学连.补阳还五汤对糖尿病闭塞性动脉硬化症的临床研究.中国医药学报，1998，13(6):21-22.
[5]马锐，赵建宛.温阳通脉汤治疗糖尿病下肢动脉硬化闭塞症120例[J].中医临床研究，2011，3（6）：13-14.
[6]李德海，余武，蔡莉莉,等.三七通舒治疗糖尿病合并下肢动脉硬化的疗效观察[J].湖北中医杂志，2007，29（5）：38-39.
[7]任志雄.糖痛方治疗早期糖尿病性动脉闭塞症的临床研究：（博士学位论文）.北京：北京中医药大学，2004.
[8]徐灿坤,曲竹秋.翻地还五汤治疗糖尿病肢体动脉闭塞症疗效观察.辽宁中医杂志，2006，33（7）：835.
[9]韩建勤,张彦宁,赵通洲,等.雷公藤治疗糖尿病下肢动脉硬化闭塞症.实用糖尿病杂志，2007，3（1）：50-51.
[10]苏立德,颜纪贤.雷化藤多甙治疗系统性硬皮病临床观察.中国中西医结合杂志，1994,4:234-235.
[11]陈星,丰美富,朱国英.雷公藤红素对血管平滑肌细胞内游离Ca2+和H+浓度的影响[J].中国中西医结合杂志,1999,19(9):538-540.
[12]刘志伟.丹红注射液治疗2型糖尿病下肢AS闭塞症68例疗效观察[J].山东中医，2007，47（28）107-108.
[13]刘艳，郭晖，杨松青,等.刺五加治疗糖尿病下肢动脉硬化闭塞症44例.吉林大学学报（医学版）,2003，29（6）：821-823.
[14]季守贤,包红.刺五加治疗糖尿病性脑梗塞疗效分析[J].中风与神经疾病杂志,1997,14(4):241.
[15]郭水英.大剂量刺五加注射液治疗周围血管病的血液流变学观察[J].实用中西医结合杂志,1993,(2):114-115.
[16]刘玉兰,王世久,蔡玉珉.刺五加茎叶对血小板聚集功能的影响[J].沈阳药学院学报,1989,6(1):57-60.
[17] Johnson GJ, Dunlop PC, Leis LA, et al. Dihydropyridine agonist Bay K8644inhibits platelet activation by competitive antagonism of thromboxaneA2-prostaglandin H2receptor. Circ Res,1988,62(3):494-505.
[18]王树立,李永德,赵勤,等.山楂、黄芪、刺五加对豚鼠胆固醇代谢的影响初报[J].河南医学情报,1987,4(8):783-785.
[19]倪劲松,吴家祥,肖幻秋,等.刺五加皂甙对糖尿病大鼠血过氧化脂质和超氧化物歧化酶的影响[J].白求恩医科大学学报,1998,24(1):33-34.
[20]罗礼东.灯盏花素注射液治疗下肢动脉硬化闭塞症38例临床观察.福建医药杂志，2005,27(6):153-154.
[21]王影,杨祥良,刘宏，等.灯盏花素抗凝作用的研究.中药材,2003,26(9):656-658.
[22]张颖,李玲妹,孙京晶,等.注射用灯盏花素治疗缺血性脑血管病43例临床观察.中华临床医药,2003,4(5):9.
[23]冯琨,谭静范,陈影,等.疏血通注射液治疗糖尿病下肢动脉硬化闭塞症临床观察.中国中西医结合杂志，2009,29(3):255-256.
[24]刘皓,崔炎,刘辉,等.中药外治糖尿病肢体动脉闭塞症.中国中西医结合外科杂志.2009,25(3):271-272.
[25]任文英,李建民,赵丹阳,等.中药外洗联合前列腺E1(PGE1)治疗糖尿病下肢动脉硬化闭塞症48例.陕西中医学院学报，2008，31（1）：35-36.
[26]郝威威.糖尿病并下肢动脉硬化闭塞症益气活血中药促进干细胞移植后血管分化的试验研究，2007，5：1-45.
[27]何晓兰.益气通脉方合外洗方治疗早期糖尿病下肢动脉硬化闭塞症的临床观察.北京中医.2005，24(4):195-196.
[28]焦海强，孙传聪.动静脉泵LBTK-M-I1000在下肢动脉硬化症患者中的应用.现代诊断与治疗，2012,23(7):985-986.
[29]刘洪涛,祖茂衡,徐浩,等.讨微波深部热疗治疗老年下肢动脉硬化闭塞症.中外医疗（临床医学），2010,31:91.
[30]赵钢,吕勃川,于文慧.巴曲酶和前列地尔治疗下肢动脉硬化闭塞症193例.中国中西医结合外科杂志，2009,15(1):45-46.
[31]李昌祁,冯佳庆,黄晓玲，等.东菱迪芙治疗糖尿病周围血管病变多项目观察附32例临床分析[J].中国医药指南,2007,5(9):38.
[32]华智强,王滨.东菱迪芙治疗糖尿病周围神经病变60例疗效观察[J].中国实用神经疾病杂志，2006,9(6):133.
[33] Kernick DP, Shore AC. Characteristics of laser Doppler perfusion imagingin vitro and in vivo. Physiol Meas,2000,21(2):333-340.
[34]姜宗,曹丽英.前列地尔在临床上的应用[J].中国老年学杂志,2003,9(23):628.
[35]莫励敏.中西医结合治疗糖尿病并下肢动脉硬化60例.中国民间疗法，2007，13（9）：6-7.
[36]丁学屏.中西医结合糖尿病学.北京:人民卫生出版社,2004年3月第1版，35-425.
[37]刘汉庆.中西医结合治疗糖尿病肢体动脉硬化性闭塞症35例.安徽中医学院学报.2009,28(1):21.
[38]姜凯,黄丽秋,高凯,等.中西医结合治疗下肢动脉硬化闭塞症47例.长春中医药大学学报，2009，25（1）：103-105.
[39]兰静.辨证施护对LASO的影响.中国中医急症，2010,19(6):1073-1074.
[1]潘长玉，高妍，袁申元，等，2型糖尿病下肢血管病变发生率及相关因索调查[J].中国糖尿病杂志，2001，5(9):323.
[2]谢铮伟.补阳还五汤加味对糖尿病闭塞性动脉硬化症的临床观察.安徽卫生职业技术学院学报，2004，3(2):21-12.
[3]张亿倬,韩继武,黄玉玲.动脉硬化超声所见与危险因子及年龄的相关性[J].中国临床康复,2005,9(41):34-36.
[4] Taddei S, Virdis A, Mattei P, et al. Aging and endothelial function innormotensive subjects and patients with essential hypertension. Circulation,1995,91（7）:1981-1987.
[5] Vander meer IM, Iglesias del Sol A, Wittenman JC, et al. Risk factors forprogression of atherosclerosis measured at multiple sites in the arterial tree:the Rotterdam Study. Stroke,2003,34(10):2374-2379.
[6]邱飞.肿瘤坏子因子α与心力衰竭的研究进展.国外医学·药学分册.2003,30(6):326-330.
[7]李小鹰，范利。老年周围动脉硬化闭塞性疾病[M]．济南：山东科学技术出版社，2003年8月第1版，1-142.
[8]胡承恒，杜志民，罗初凡，等．年龄与性别在冠状动脉钙化程度和冠心病的诊断价值中的影响[J]．中华心血管病杂志，2001，29（11）：668-671.
[9] Grodstein F，Stampfer MJ，Cobditz GA，et a1．Postmenopausal Hormone Therapyand Mortality. N Engl J Med，1997，337(19)：1389-1391.
[10]阮云军，吴赛珠，孟素荣，等.雌激素对血管内皮细胞一氧化氮合成酶活性调控的受体机制研究.中华老年心脑血管病杂志，2000,2(4):263-265.
[11]染春卉，梁伯平，张晶.绝经期女性雌激素水平与血脂关系分析.临床心血管病杂志，1999,15(5)：232.
[12]叶文翔编著.脑血管疾病.北京：中国医药科技出版社,1990年3月第1版,110.
[13]陈兴洲译.吸烟是卒中的危险因素.国外医学脑血管疾病分册，1995，3(3):122.
[14]马温良,王艳,陈荣杰，等.吸烟与动脉硬化性脑梗塞关系的研究[J].中国慢性病预防与控制，1999,7(3):101.
[15]赵忠信，王彦华.血液高凝状态的相关因素[J].现代诊断与治疗，1998,9(6):381-382.
[16] Jackson WF. Quick change artist: endothelium-derived relaxing factor inresistance arteries. Hypertansion,2011,57(4):686-688.
[17]邓发达，戴亚，朱立军，等.卷烟烟气中一氧化氮研究进展.烟草科技／烟草化学，2004,11(208):24.
[18]张育，郑诚东，张代民，等.吸烟对健康人血清HDL-C等7项指标水平影响的对比观察[J].中华流行病学杂志，1992,13（2）：97.
[19] Wallis WJ, Beatty PG, Ochs HD, et al. Human monocyte adherence to culturedvascular endothelium: monoclonal antibody-defined mechanisms. J Immunol,1985,135(4):2323-2330.
[20] Willett W, Hennekens CH, Castelli W, et al. Effects of cigarette smokingon fasting triglyceride, total cholesterol, and HDL-cholesterol in women. AmHeart J,1983,105(3):417-421.
[21]毕小云，邓小玲，肖琴，等.吸烟对血脂的影响[J].重庆医科大学学报，2004,29(1):80-82.
[22] Kong C，Nimmo L，Elatrozy T, et al. Smoking is associated with increasedhepatic lipase activity, insulin resistance, dyslipidaemia and earlyatherosclerosis in Type2diabetes. Atherosclerosis,2001,156(2):373-378.
[23]念馨,张旭祥,宋滇平.2型糖尿病下肢血管病变相关因素分析.中华临床医师杂志，2007,1(5):33-34.
[24]赵水平．临床血脂学[M]．北京：人民卫生出版社，2006年12月第1版，11-234.
[25] Piantadosi CA, Schwartz DA. The acute respiratory distress syndrome. AnnIntern Med,2004,141(6):460-470.
[26] Puneet P, Moochhala S, Bhatia M. Chemokines in acute respiratory distresssyndrome. Am J Physiol Lung Cell Mol Physiol,2005,288(1):L3-L15.
[27]刘莉，叶鹏.SBP变异性与2型糖尿病患者糖尿病肾病及动脉粥样硬化相关.中华高血压杂志，2012，6（20）:599-560.
[28]刘燕.2型糖尿病合并高血压LASO危险因素分析[J].现代诊断与治疗，2012,23(6):841.
[29]侯德凤.血脂和载脂蛋白ApoA1、ApoB的测量与糖尿病合并血管病变的关系［J］.华夏医学，2000，13（3）：360.
[30]马绍杰，王颖，金秀平.2型糖尿病大血管病变相关因素分析.华北煤炭医学院学报，2004,6(4):446-447.
[31]赵水平.糖尿病血脂异常及治疗.中华内科杂志,2002,41(5):356-358.
[32]黄峻，刘超，丁国宪．代谢综合征与心血管疾病[M]．北京：科学出版社，2004年5月第1版，232-236.
[33]洪华山,刘翼,王一波,等.糖基化低密度脂蛋白增加血管内皮对单核细胞的粘附作用.中华内分泌代谢杂志,1998,4(14):48-50.
[34]刘秉文，曾成林.高密度脂蛋白抗AS作用[J],中国动脉硬化志，1994,2(1):45-47.
[35] Fernandez ML, McNamara DG. High-density lipoprotein binding to guinea-pighepatic membranes. Comparison of guinea-pig and human ligands. Biochim BiophysActa,1990，1042(1):142-145.
[36] Brinton EA, Oram JF, Chen CH, et a1．Binding of high density lipoproteinto cultured fibroblasts after chemical alteration of apoprotein amino acidresidues. J Biol Chem,1986，261(1)：495-503.
[37] Chajek T, Aron L, Fielding CJ．Interaction of lecithin: cholesterolacyltransferase and cholesteryl ester transfer protein in the transport ofcholesteryl ester into sphingomyelin liposomes. Biochemistry,1980,19(16)：3673-3677.
[38] Shastri KM, Carvalho AC, Lees RS, et a1．Platelet function and plateletlipid composition in the dyslipoproteinemias. Lipid Res，1980，21(4):467-472.
[39]王锦淳.黄芩茎叶总黄酮对高甘油三酯诱导的血管内皮细胞氧化损伤的保护作用及机制研究.扬州大学学报，2012,38(3):397-340.
[40] Keaney JF Jr. Oxidative stress and the vascular wall: NADPH oxidases takecenter stage. Circulation,2005,112(17):2585-2588.
[41]廖志红，余斌杰．2型糖尿病血脂代谢紊乱及其控制[J]．中华内分泌杂志，2002，14(4)：277．
[42] Jandeleit-Dahm K, Cooper ME. The role of AGEs in cardiovascular disease.Curr Pharm Des,2008,14(10):979-986.
[43] Duh E, Aiello LP. Vascular endothelial growth factor and diabetes: theagonist versus antagonist paradox. Diabetes,1999,48(10):1899-1906.
[44] Shoji T, Koyama H, Morioka T, et al. Receptor for advanced glycation endproducts is involved in impaired angiogenic response in diabetes. Diabetes,2006,55(8):2245-2255.
[45] Renard C, Chappey O, Wautier MP, et al. Recombinant advanced glycation endproduct receptor pharmacokinetics in normal and diabetic rats.. Mol Pharmacol,1997,52(1):54-62.
[46] Wautier MP, Chappey O, Corda S, et al. Activation of NADPH oxidase by AGElinks oxidant stress to altered gene expression via RAGE. Am J Physiol EndocrinolMetab,2001,280(5): E685-E694.
[47] Ahmad FK, He Z, King GL. Molecular targets of diabetic cardiovascularcomplications. Curr Drug Targets,2005,6(4):487-494.
[48] Hammes HP. Pathophysiological mechanisms of diabetic angiopathy. J DiabetesComplications,2003,17(2Suppl):16-19.
[49] Anderson HD, Rahmutula D, Gardner DG. Tumor necrosis factor-alpha inhibitsendothelial nitric-oxide synthase gene promoter activity in bovine aorticendothelial cells. J Biol Chem,2004,279(2):963-969.
[50] Evans JL, Goldfine ID, Maddux BA, et al. Are oxidative stress-activatedsignaling pathways mediators of insulin resistance and beta-cell dysfunction?Diabetes,2003,52(1):1-8.
[53] Johansen JS, Harris AK, Rychly DJ, et al. Oxidative stress and the use ofantioxidants in diabetes: linking basic science to clinical practice. CardiovascDiabetol,2005,4(1):5.
[51] Maritim AC, Sanders RA, Watkins JB3rd. Diabetes, oxidative stress, andantioxidants: a review. J Biochem Mol Toxicol,2003,17(1):24-38.
[52] Patterson RA, Horsley ET, Leake DS. Prooxidant and antioxidant propertiesof human serum ultrafiltrates toward LDL: important role of uric acid. J LipidRes,2003,44(3):512-521.
[53] Sanguinetti SM, Batthyany C, Trostchansky A, et al. Nitric oxide inhibitsprooxidant actions of uric acid during copper-mediated LDL oxidation.. ArchBiochem Biophys,2004,423(2):302-308.
[54]孙海鸥.尿酸与AS关系的基础与临床初步研究：（硕士研究生毕业论文），第四军医大学.
[55] Nakagawa T, Zharikov S, Tuttle KR, et al. A causal role for uric acid infructose-induced metabolic syndrome. Am J Physiol Renal Physiol,2006,290(3):F625-631.
[56] Kanellis J, Kang DH. Uric acid as a mediator of endothelial dysfunction,inflammation and vascular disease.Semin Nephrol,2005,25(1):39-42.
[57] Leyva F, Anker S, Swan JW et al. Serum uric acid as an index of impairedoxidative metabolism in chronic heart failure. Eur Heart J,1997,18(5):858-865.
[58]张福琴，李志超，赵德,等.5-羟色胺在野百合碱引起大鼠肺动脉高压发病中的作用.中国病理生理杂志,1999,15（5）:462-466.
[59]彭荔薰，冯波. NIDDM患者血浆组织型纤维蛋白溶酶原激活物及其抑制物活性水平与胰岛素抵抗的探讨.中华内分泌代谢杂志,1995.2(3):110-112.
[60] Kawamoto R, Tomita H, Oka Y, et al. Association between uric acid and carotidatherosclerosis in elderly persons. Intern Med,2005,44(8):787-793.
[61]余振球，赵连友，刘国杖.高血压防治进展与实践［M］.北京:科学出版社，2003年1月第1版，254.
[62]张敏.Ⅱ型糖尿病患者血尿酸水平与血管并发症的相关性研究.中国实用医药，2011，6（14）:1131-1134.
[63]宫国东，宁为民，林家东.高尿酸血症与动脉硬化性脑梗死的关系研究.吉林医学，2010,31（24）：4065.
[64] Farquharson CA, Butler R, Hill A, et al. Allopurinol improves endothelialdysfunction in chronic heart failure. Circulation,2002,106(2):221-226.
[65] Doehner W, Schoene N, Rauchhaus M, et al. Effects of xanthine oxidaseinhibition with allopurinol on endothelial function and peripheral blood flowin hyperuricemic patients with chronic heart failure: results from2placebo-controlled studies. Circulation,2002,105(22):2619-2624.
[66]王雪青，刘乃奎，董林旺，等．纤维蛋白原在AS中的作用[J]．中国病理生理杂志，1997，3(3)：270-273.
[67] Sato S，Nakamura N，Iida M，et a1．Plasma fibrinogen and coronary heartdisease in urban Japanese. Am J Epidemiol，2000，152(5)：420-423.
[68] Loukas M，Dabrowski M，Wagner T，et a1．Fibrinogen and smooth muscle celldetection in atherosclerotic plaques from stable and unstable angina-animmunohistochemical study．Med Sci Monit，2002，8(4):BR144-148.
[69] Fibrinogen Studies Collaboration．Danesh J, Lewington S, Thompton SG, etal. Plasma fibrinogen level and the risk of major cardiovascular diseases andnonvascular mortality: an individual participant meta-analysis．JAMA，2005，294(14)：1799-1809.
[70]王洁，李小鹰，何耀，等．老年周围动脉硬化闭塞病与血浆纤维蛋白原、血小板集聚率关系的研究[J]．中华流行病学杂志，2005，26(1)：l-4.
[71]李丽,高大胜.血浆纤维蛋白原与冠状AS性心脏病的相关性研究[J].实用全科医学,2008,6(3):228-229.
[72] Lind P, Hedblad B, Stavenow L, et al. Influence of plasma fibrinogen levelson the incidence of myocardial infarction and death is modified by otherinflammation-sensitive proteins: a long-term cohort study.. Arterioscler ThrombVasc Biol,2001,21(3):452-458.
[73] Mortensen RF, Zhong W. Regulation of phagocytic leukocyte activities byC-reactive protein. J Leukoc Biol,2000,67(4):495-500.
[74] Zhang YX, Cliff WJ, Schoefl GI, et al. Coronary C-reactive proteindistribution: its relation to development of atherosclerosis.. Atherosclerosis,1999,145(2):375-379.
[75] Verma S, Wang CH, Li SH, et al. A self-fulfilling prophecy: C-reactiveprotein attenuates nitric oxide production and inhibits angiogenesis.Circulation,2002,106(8):913-919.
[76] Torzewski J. C-reactive protein and atherogenesis: new insights fromestablished animal models. Am J Pathol,2005,167(4):923-925.
[77] Zwaka TP, Hombach V, Torzewski J. C-reactive protein-mediated low densitylipoprotein uptake by macrophages: implications for atherosclerosis. Cirulation,2001,103(9):1194-1197.
[78]潘清蓉,孙梅励. C反应蛋白在AS中的作用[J].基础医学与临床,2004,24(4):462-465.
[79] Wang CH, Li SH, Weisel RD, et al. C-reactive protein upregulates angiotensintype1receptors in vascular smooth muscle[J]. Circulation,2003,107(13):1783-1790.
[80] Devaraj S, Xu DY, Jialal I, et al. C-reactive protein increases plasminogenactivator inhibitor-1expression and activity in human aortic endothelial cells:implications for the metabolic syndrome and atherothrombosis[J].Circulation,2003,107(3):398-404.
[1]杨文英等.中国2型糖尿病防治指南.北京：北京大学医学出版社.2011年9月第1版，3-50.
[2]张亿倬,韩继武,黄玉玲.动脉硬化超声所见与危险因子及年龄的相关性[J].中国临床康复,2005,9(41):34-36.
[3] Taddei S, Virdis A, Mattei P, et al. Aging and endothelial function innormotensive subjects and patients with essential hypertension. Circulation,1995,91(7):1981-1987.
[4] Vander meer IM, Iglesias del Sol A, Wittenman JC, et al. Risk factorsfor progression of atherosclerosis measure at multiple sites in the arterialtree: the Rotterdam Study.Stroke,2003,34(10):2374-2379.
[5]邱飞.肿瘤坏子因子α与心力衰竭的研究进展.国外医学·药学分册，2003,30(6):326-330.
[6] Asakawa H, Toktmaga K, Kawakami F. Comparison of risk factors ofmacrovascular comp lications peripheral vascular disease, cembral vasculardisease, and coronary heart dlsease in Japanes type2diabetes mellitus patients.J Diabetes Comp,2000,14(4):307-313.
[7]念馨,张旭祥,宋滇平.2型糖尿病下肢血管病变相关因素分析.中华临床医师杂志，2007,1(5):33-34.
[8] Piantadosi CA, Schwartz DA. The acute respiratory distress syndrome. AnnIntern Med,2004,141(6):460-470.
[9] Puneet P, Moochhala S, Bhatia M, Chemokines in acute respiratory distresssyndrome. Am J Physiol Lung Cell Mol Physiol,2005,288(1):L3-L5.
[10]刘莉，叶鹏.SBP变异性与2型糖尿病患者糖尿病肾病及AS相关.中华高血压杂志，2012，6（3）：65-67.
[11]刘燕.2型糖尿病合并高血压LASO危险因素分析[J].现代诊断与治疗，2012,23(6):841.
[12] Levenson JA, Simon AC, Safar ME, et al. Systolic hypertension inarteriosclerosis obliterans of the lower limbs. Clin Exp Hypertens A,1982,4(7):1059-1072.
[13] Nakagawa T, Zharikov S, Hu H, et al. A causal role for uric acid infructose-induced metabolic syndrome. Am J Physiol Renal Physiol,2006,290(3):F625-F631.
[14] Kanellis J, Kang DH. Uric acid as a mediator of endothelial dysfunction,inflammation and vascular disease. Semin Nephrol,2005,25(1):39-42.
[15] Leyva F, Anker S, Swan JW, et al. Serum uric acid as an index of impairedoxidative metabolism in chronic heart failure.. Eur Heart J,1997,18(5):858-865.
[16]张福琴，李志超，赵德，等.5-羟色胺在野百合碱引起大鼠肺动脉高压发病中的作用.中国病理生理杂志,1999，5（15）：1120-1123.
[17]彭荔薰，冯波. NIDDM患者血浆组织型纤维蛋白溶酶原激活物及其抑制物活性水平与胰岛素抵抗的探讨.中华内分泌代谢杂志,1995.2（4）：110-112.
[18] Kawamoto R, Tomita H, Oka Y. Association between uric acid and carotidatherosclerosis in elderly persons.Intern Med,2005,44(8):787-793.
[19]余振球，赵连友，刘国杖.高血压防治进展与实践［M］.北京:科学出版社，2003年1月第1版，254.
[20]张敏.Ⅱ型糖尿病患者血尿酸水平与血管并发症的相关性研究.中国实用医药，2011，6（14）：1131-1134.
[21]宫国东，宁为民，林家东.高尿酸血症与动脉硬化性脑梗死的关系研究.吉林医学，2010，31（24）：4065.
[22] Farquharson CA, Butler R, Hill A, et al. Allopurinol improves endothelialdysfunction in chronic heart failure.. Circulation,2002,106(2):221-226.
[23] Doehner W, Schoene N, Rauchhaus M, et al. Effects of xanthine oxidaseinhibition with allopurionl on endothelail function and peripheral blood flowin hyperuricemic patients with chronic heart failure: results from2placebo-controlled studies. Circulation,2002,105(22):2619-2624.
[24]叶文翔编著.脑血管疾病.北京：中国医药科技出版社,1990年3月第1版,110.
[25]陈兴洲译.吸烟是卒中的危险因素.国外医学脑血管疾病分册，1995，3(3):122.
[26]马温良,王艳,陈荣杰，等.吸烟与动脉硬化性脑梗塞关系的研究[J].中国慢性病预防与控制.1999,7(3):101.
[27]赵忠信，王彦华.血液高凝状态的相关因素[J].现代诊断与治疗，1998,9(6):381-382.
[28] Jackson WF. Quick change artist: endothelium-derived relaxing factor inresistance arteries. Hypertension,2011,57(4):686-688.
[29]邓发达，戴亚，朱立军，等.卷烟烟气中一氧化氮研究进展.烟草科技／烟草化学，2004,11(208):24.
[30]张育，郑诚东，张代民，等.吸烟对健康人血清HDL-C等7项指标水平影响的对比观察[J].中华流行病学杂志，1992,13（2）：97.
[31] Wallis WJ, Beatty PG, Ochs HD, et al. Human monocyte adherence to culturedvascular endothelium: monoclonal antibody-defined mechanisms. J Immunol,1985,135(4):2323-2330.
[32] Willett W, Hennekens CH, Castelli W, et al. Effects of cigarette smokingon fasting triglyceride, total cholesterol, and HDL-cholesterol in women. AmHeart J,1983,105(3):417-421.
[33]毕小云，邓小玲，肖琴等.吸烟对血脂的影响[J].重庆医科大学学报，2004,29(1):80-82.
[34] Kong C，Nimmo L，Elatrozy T, et al. Smoking is associated with increasedhepatic lipase activity, insulin resistance, dyslipidaemia and earlyatherosclerosis in Type2diabetes. Atheroclerosis,2001,156(2):373-378.
[35]刘秉文，曾成林.高密度脂蛋白抗AS作用[J].中国动脉硬化志，1994,2(1):45-47.
[36] Fernandez ML, McNamara DG. High-density lipoprotein binding to guinea-pighepatic membranes. Comparison of guinea-pig and human ligands. Biochim BiophysActa,1990，1042(1):142-145.
[37] Brinton EA, Oram JF, Chen CH, et a1．Binding of high density lipoproteinto cultured fibroblasts after chemical alteration of apoprotein amino acidresidues. J Biol Chem,1986，261(1)：495-503.
[38] Chajek T, Aron L, Fielding CJ．Interaction of lecithin: cholesterolacyltransferase and cholesteryl ester transfer protein in the transport ofcholesteryl ester into sphingomyelin liposomes. Biochemistry,1980,19(16)：3673-3677.
[39] Shastri KM, Carvalho AC, Lees RS, et a1．Platelet function and plateletlipid composition in the dyslipoproteinemias. Lipid Res，1980，21(4):467-472.
[1]潘长玉，高妍，袁申元，等，2型糖尿病下肢血管病变发生率及相关因索调查[J].中国糖尿病杂志，2001,(9)：323.
[2]中国中西医结合学会周围血管疾病专业委员会.糖尿病肢体动脉闭塞症诊断及疗效标准(草案).中西医结合心脑血管病杂志，2004(6)，2(6):352.
[3]陈淑长，葛苋主编．周围血管病的研究进展与中医治疗经验．北京：学苑出版社，2002年1月第1版，259-260.
[4]高雪敏主编.中药学.北京：中国中医药出版社，2002年9月第1版，364-366.
[5]雷载权主编.中药学.上海：上海科学技术出版社出版.1998年6月第1版，307-308.
[6]崔艳君，陈若芸.鸡血藤化学和药理研究进展.天然产物研究与开发，2006，15(4):72.
[7]仇锦春，卞慧敏.通塞脉片对大鼠实验性高脂血症及AS的影响[J].上海中医药杂志，2007，41（1）：71-73.
[8]顾锡镇.通塞脉片治疗急性脑缺血性中风30例.南京中医药大学学报，2004，20（2）：831.
[9]杨军，屈立志.通塞脉片对深静脉血栓形成纤溶功能的实验观察[J].中药新药与临床药理，2003，4（1）：32-33.
[10]姜淼，卞慧敏.通塞脉片对AS模型大鼠的影响[J].新中医，2007，39（12）：102-104.
[11]徐婷，王微.牛膝水煎液对自发性高血压大鼠血压和左心室肥厚的影响[J].长春中医药大学学报，2008，24（4）：367-368.
[12] Chen H, Li D, Sawamura T, et al. Upregulation of LOX-1expression in aortaof hypercholesterolemic rabbits: modulation by losartan. Biochem Biophys ResCommon,2000,276(3):1100-1104.
[13]李敏，孙虹，李琰.不同产地当归对血小板聚集及凝血时间活性的比较.中国中医基础医学杂志，2003，9（2）：47-50.
© 2004-2018 中国地质图书馆版权所有 京ICP备05064691号 京公网安备11010802017129号 地址：北京市海淀区学院路29号 邮编：100083 电话：办公室：(+86 10)66554848；文献借阅、咨询服务、科技查新：66554700 |