布托啡诺对大鼠感染性休克和心肌缺血再灌注损伤炎性反应的研究
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摘要
第一部分布托啡诺对感染性休克大鼠血流动力学及炎性细胞因子的影响
目的探讨布托啡诺对感染性休克大鼠的血流动力学指标及血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)的影响。
方法取健康雄性SD大鼠40只,随机分为4组(n=10)：假手术组(C组)、手术组(CLP组)、手术加布托啡诺组(CLP+B组)、假手术加布托啡诺组(B组)。腹腔注射20%乌拉坦1 g·kg-1麻醉后,分离左侧股静脉置入22G套管针以备输注布托啡诺或生理盐水。CLP组、CLP+B组分别注射生理盐水5ml·kg-1和布托啡诺0.5 mg·kg-1后30分钟采用盲肠结扎加穿孔法(CLP)制备感染性休克模型,C组、B组分别注射生理盐水5 ml·kg-1和布托啡诺0.5mg·kg-1而不行CLP。分离各组大鼠右侧股动脉置管监测平均动脉压(MAP)和心率(HR),并分别于CLP后4h、12h和20h经右侧股动脉采血1 ml,采用酶联免疫吸附试验检测肿瘤细胞因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)浓度。
结果CLP组MAP呈进行性下降,HR先快后慢,CLP+B组MAP下降幅度较小,HR波动小,CLP组和CLP+B组血清TNF-α和IL-6水平于CLP后各时点呈先增高后降低的趋势,并高于其余各组(P<0.05),且CLP组高于CLP+B组(P<0.05)；CLP组和CLP+B组血清IL-10水平于CLP后4h后呈上升趋势,并高于其余各组(P<0.05),且CLP+B组高于CLP组(P<0.05)；B组血流动力学指标及各细胞因子水平与C组比较无差异(P>0.05)。
结论布托啡诺通过降低血清促炎性细胞因子TNF-α和IL-6,增加抗炎性细胞因子IL-10浓度对感染性休克大鼠血流动力学稳定方面起到保护作用,而对正常大鼠血流动力学指标及细胞因子无影响作用。
第二部分布托啡诺对在体大鼠心肌缺血再灌注损伤作用的研究
目的探讨布托啡诺对大鼠心肌缺血再灌注损伤的影响。
方法健康雄性SD大鼠40只,体重200～250 g,随机分为5组,每组8只。假手术组(A组)：左冠状动脉前降支(LAD)处只穿线不结扎。缺血/再灌注组(B组)：左冠状动脉前降支处穿线结扎30 min后,松开结扎线再灌注120 min。A、B组在缺血前10 min经股静脉注射生理盐水5ml·kg-1后以5ml·kg-1·h-1持续静脉输注至实验结束。布托啡诺低剂量组(C组)：缺血前10 min经股静脉注射布托啡诺25μg·kg-1,余处理同B组；布托啡诺中剂量组(D组)：缺血前10 min经股静脉注射布托啡诺50μg·kg-1,余处理同B组；布托啡诺高剂量组(E组)缺血前10 min经股静脉注射布托啡诺100μg·kg-1,余处理同B组。
腹腔注射20%乌拉坦1 g·kg-1麻醉后,气管切开行机械通气,分离左侧股静脉置入22G套管针以备输注布托啡诺或生理盐水,分离右侧股动脉置管监测平均动脉压(MAP)和心率(HR)。再灌注结束后,取心肌组织测心肌梗死范围,光镜观察心肌组织结构；取大鼠心肌缺血区组织测定丙二醛(MDA)水平。
结果与缺血/再灌注组比较,布托啡诺处理各组心肌梗死范围减少(P<0.05),随着布托啡诺使用剂量的增加,心肌梗死范围逐渐减小,各浓度布托啡诺处理组之间差异具有统计学意义(P<0.05)；缺血/再灌注组心肌组织结构明显损害,布托啡诺低剂量组心肌组织结构损害程度较缺血/再灌注组轻,布托啡诺中剂量组和高剂量组心肌组织结构更接近于正常A组。与A组比较,其余各组心肌组织丙二醛含量均有增加(P<0.05)；与缺血/再灌注组比较,布托啡诺处理各组心肌组织丙二醛含量降低(P<0.05)；随着布托啡诺使用剂量的增加,心肌组织丙二醛含量逐渐减小,各浓度布托啡诺处理组之间差异具有统计学意义(P<0.05)。
结论布托啡诺可减少大鼠心肌缺血再灌注损伤后心肌梗死范围,减轻大鼠心肌缺血再灌注时心肌组织结构损伤程度,降低心肌缺血再灌注损伤后心肌组织丙二醛含量,对在体大鼠心肌缺血再灌注损伤有保护作用。
第三部分炎性细胞因子在布托啡诺对大鼠心肌缺血再灌注损伤作用中的影响及其机制
目的探讨炎性细胞因子在布托啡诺对大鼠心肌缺血再灌注损伤保护作用中的作用及其机制。
方法健康雄性SD大鼠40只,体重200～250 g,随机分为5组,每组8只。假手术组(A组)：左冠状动脉前降支处只穿线不结扎。缺血/再灌注组(B组)：左冠状动脉前降支(LAD)处穿线结扎30 min后,松开结扎线再灌注120min。A、B组在缺血前10 min经股静脉注射生理盐水5 ml·kg-1后以5 ml·kg-1·h-1持续静脉输注至实验结束；布托啡诺组(C组)：缺血前10 min经股静脉注射布托啡诺25μg·kg-1,其它处理同B组；Nor-BNI组(D组)：缺血前20 min经股静脉注射选择性K阿片受体阻断剂Nor-BNI 2 mg·kg-1,余处理同C组；glibenclamide组(E组)：缺血前10 min经股静脉注射KATP通道阻断剂glibenclamide 1 mg·kg1余处理同C组。
实验动物腹腔注射20%乌拉坦1 g·kg-1麻醉后,分离左侧股静脉置入22G套管针,以备输注布托啡诺或生理盐水；连续监测Ⅱ导心电图；气管切开,连接动物呼吸机行机械通气。再灌注结束后,通过股动脉置管收集血样本测定血清TNF-α、IL-6和IL-10的浓度。
结果与假手术组比较,其余各组血清TNF-α、IL-6和IL-10浓度均明显上升(P<0.01)；与缺血/再灌注比较,布托啡诺处理各组血清TNF-α、IL-6浓度降低(P<0.05),IL-10浓度增高(P<0.05)；与布托啡诺组相比,Nor-BNI组和glibenclamide组血清TNF-α、IL-6浓度增高(P<0.05),IL-10浓度降低(P<0.05)
结论布托啡诺可降低大鼠心肌缺血再灌注时促炎性细胞因子的浓度并增加抗炎性细胞因子的浓度,且布托啡诺对这种炎性细胞因子的保护作用部分是通过心肌组织K阿片受体和KATP通道所产生的。
PART 1 Effects of butorphanol tartrate on inflammatory response in septic rats
Objective:To investigate the effects of butorphanol tartrate on inflammatory cytokines in septic rats.
Methods:Forty adult male SD rats weighing 200～250 g were randomly divided into sham-operated group (group C), operated group (group CLP), operated and butorphanol group (group CLP+B) and butorphanol group(group B). Septic shock model was induced by cecal ligation puncture (CLP). Thirty minutes before CLP 5 ml·kg-1 saline and 0.5 mg·kg-1 butorphanol were injected intravenously in group CLP and group CLP+B respectively. Group C and group B only received saline (5 ml·kg-1) and butorphanol (0.5 mg·kg-1) respectively. Mean artery pressure (MAP) and heart rate (HR) were monitored via the right femoral artery. Tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10) in serum were measured at 4 h,12 h and 20 h after CLP.
Results:MAP decreased progressively after CLP in group CLP and group CLP+B, while HR increased at first and decreased afterwards in group CLP. The decrease of MAP was inhibited, and the changes of HR were slight in group CLP+B. TNF-α, IL-6 and IL-10 concentrations in group CLP were higher than those in group C at 4,12 and 20 hours after CLP (P<0.05). TNF-a and IL-6 concentrations in group CLP+B were lower than those in group CLP(P<0.05).IL-10 concentrations in group CLP+B were higher than those in group CLP(P<0.05). There were no significant effects on TNF-α、IL-6 and IL-10 concentrations between group C and group B(P>0.05).
Conclusions:Butorphanol tartrate has protective effects on septic shock rats by decreasing pro-inflammatory cytokines TNF-α, IL-6 concentrations and increasing anti-inflammatory cytokine IL-10 concentrations. Butorphanol tartrate has no significant effect on the TNF-α, IL-6 and IL-10 concentrations of normal rats.
PART 2 Effects of butorphanol tartrate on myocardial ischemia reperfusion injury in rats
Objective To observe the effects of butorphanol on myocardial infarct size,malondialdehyde and myocardial structure following myocardial ischemia-reperfusion (I/R) in rats.
Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into five groups with 8 in each group:control group(group A);I/R group(group B); low dosage butorphanol group (group C); moderate dosage butorphanol group(group D) and high dosage butorphanol group(group E). In group B,C,D and E myocardial ischemia-reperfusion was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion.In group C,D and E butorphanol 25μg·kg-1,50μg·kg-1and 100μg·kg-1 was given respectively IV 10 min before occlusion of LAD. The myocardial infarct size was determined by TTC method and the changes of myocardial microstructure were observed under light-microscope. The tissue concentrations of malondialdehyde were measured.
Results The myocardial infarct sizes were both significantly reduced in all butorphanol groups compared with those in I/R group (P<0.05), and myocardial infarct sizes in high dosage butorphanol group were lower than those in low dosage butorphanol group. The myocardial structures of rats in all butorphanol groups were better than those in I/R group, and in moderate dosage butorphanol group and high dosage butorphanol group the myocardial structures were generally normal. Concentrations of malondialdehyde in myocardial ischemia-reperfusion groups were higher than those in control group (P<0.05),Malondialdehyde concentrations in all butorphanol groups were reduced compared with those in I/R group (P<0.05).
Conclusion Butorphanol provide a protective effect on rat heart in a dose-dependent manner following myocardial ischemia-reperfusion.
PART 3 Effects and mechanisms of butorphanol tartrate on inflammatory response in myocardial ischemia-reperfusion rats
Objective To investigate the effect and mechanism of butorphanol tartrate on inflammatory cytokines in myocardial ischemia-reperfusion(I/R) rats.
Methods Forty healthy male SD rats weighing 200～250 g were randomly divided into 5 groups (n=8):control group (group A); I/R group (group B); butorphanol group (group C); Nor-BNI group (group D) and glibenclamide group (group E). In group B,C,D and E myocardial ischemia-reperfusion was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group C,D and E butorphanol 25μg·kg-1 was givenⅣ10min before occlusion of LAD.In group D Nor-BNI 2mg·kg-1 was given IV 20 min before occlusion of LAD.In group E glibenclamide 1 mg·kg-1 was given IV 10 min before occlusion of LAD.In group A and B butorphanol were replaced by normal saline 5 ml·kg-1 followed 5 ml·kg-1-h-1. Blood samples were taken at 120 min of reperfusion for determination of serum TNF-α·IL-6 and IL-10 concentrations.
Result Compared with control group, the concentrations of TNF-a,IL-6 and IL-10 were increased in all myocardial ischemia-reperfusion groups (P <0.01).Compared with I/R group, TNF-αand IL-6 concentrations were decreased and IL-10 concentrations were increased in all butorphanol groups (P<0.05). Compared with butorphanol group, TNF-αand IL-6 concentrations were higher and IL-10 concentration was lower than those in Nor-BNI group and glibenclamide group (P <0.05).
Conclusion Serum TNF-αIL-6 and IL-10 levels were increased following myocardial ischemia reperfusion. Butorphanol decrease pro-inflammatory cytokines TNF-α, IL-6 concentrations and increase anti-inflammatory cytokine IL-10 concentrations. And the effects on cytokines of butorphanol may be attenuated by Nor-BNI or glibenclamide.
目的探讨布托啡诺对感染性休克大鼠的血流动力学指标及血清肿瘤坏死因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)的影响。
方法取健康雄性SD大鼠40只,随机分为4组(n=10)：假手术组(C组)、手术组(CLP组)、手术加布托啡诺组(CLP+B组)、假手术加布托啡诺组(B组)。腹腔注射20%乌拉坦1 g·kg-1麻醉后,分离左侧股静脉置入22G套管针以备输注布托啡诺或生理盐水。CLP组、CLP+B组分别注射生理盐水5ml·kg-1和布托啡诺0.5 mg·kg-1后30分钟采用盲肠结扎加穿孔法(CLP)制备感染性休克模型,C组、B组分别注射生理盐水5 ml·kg-1和布托啡诺0.5mg·kg-1而不行CLP。分离各组大鼠右侧股动脉置管监测平均动脉压(MAP)和心率(HR),并分别于CLP后4h、12h和20h经右侧股动脉采血1 ml,采用酶联免疫吸附试验检测肿瘤细胞因子-α(TNF-α)、白细胞介素-6(IL-6)和白细胞介素-10(IL-10)浓度。
结果CLP组MAP呈进行性下降,HR先快后慢,CLP+B组MAP下降幅度较小,HR波动小,CLP组和CLP+B组血清TNF-α和IL-6水平于CLP后各时点呈先增高后降低的趋势,并高于其余各组(P<0.05),且CLP组高于CLP+B组(P<0.05)；CLP组和CLP+B组血清IL-10水平于CLP后4h后呈上升趋势,并高于其余各组(P<0.05),且CLP+B组高于CLP组(P<0.05)；B组血流动力学指标及各细胞因子水平与C组比较无差异(P>0.05)。
结论布托啡诺通过降低血清促炎性细胞因子TNF-α和IL-6,增加抗炎性细胞因子IL-10浓度对感染性休克大鼠血流动力学稳定方面起到保护作用,而对正常大鼠血流动力学指标及细胞因子无影响作用。
第二部分布托啡诺对在体大鼠心肌缺血再灌注损伤作用的研究
目的探讨布托啡诺对大鼠心肌缺血再灌注损伤的影响。
方法健康雄性SD大鼠40只,体重200～250 g,随机分为5组,每组8只。假手术组(A组)：左冠状动脉前降支(LAD)处只穿线不结扎。缺血/再灌注组(B组)：左冠状动脉前降支处穿线结扎30 min后,松开结扎线再灌注120 min。A、B组在缺血前10 min经股静脉注射生理盐水5ml·kg-1后以5ml·kg-1·h-1持续静脉输注至实验结束。布托啡诺低剂量组(C组)：缺血前10 min经股静脉注射布托啡诺25μg·kg-1,余处理同B组；布托啡诺中剂量组(D组)：缺血前10 min经股静脉注射布托啡诺50μg·kg-1,余处理同B组；布托啡诺高剂量组(E组)缺血前10 min经股静脉注射布托啡诺100μg·kg-1,余处理同B组。
腹腔注射20%乌拉坦1 g·kg-1麻醉后,气管切开行机械通气,分离左侧股静脉置入22G套管针以备输注布托啡诺或生理盐水,分离右侧股动脉置管监测平均动脉压(MAP)和心率(HR)。再灌注结束后,取心肌组织测心肌梗死范围,光镜观察心肌组织结构；取大鼠心肌缺血区组织测定丙二醛(MDA)水平。
结果与缺血/再灌注组比较,布托啡诺处理各组心肌梗死范围减少(P<0.05),随着布托啡诺使用剂量的增加,心肌梗死范围逐渐减小,各浓度布托啡诺处理组之间差异具有统计学意义(P<0.05)；缺血/再灌注组心肌组织结构明显损害,布托啡诺低剂量组心肌组织结构损害程度较缺血/再灌注组轻,布托啡诺中剂量组和高剂量组心肌组织结构更接近于正常A组。与A组比较,其余各组心肌组织丙二醛含量均有增加(P<0.05)；与缺血/再灌注组比较,布托啡诺处理各组心肌组织丙二醛含量降低(P<0.05)；随着布托啡诺使用剂量的增加,心肌组织丙二醛含量逐渐减小,各浓度布托啡诺处理组之间差异具有统计学意义(P<0.05)。
结论布托啡诺可减少大鼠心肌缺血再灌注损伤后心肌梗死范围,减轻大鼠心肌缺血再灌注时心肌组织结构损伤程度,降低心肌缺血再灌注损伤后心肌组织丙二醛含量,对在体大鼠心肌缺血再灌注损伤有保护作用。
第三部分炎性细胞因子在布托啡诺对大鼠心肌缺血再灌注损伤作用中的影响及其机制
目的探讨炎性细胞因子在布托啡诺对大鼠心肌缺血再灌注损伤保护作用中的作用及其机制。
方法健康雄性SD大鼠40只,体重200～250 g,随机分为5组,每组8只。假手术组(A组)：左冠状动脉前降支处只穿线不结扎。缺血/再灌注组(B组)：左冠状动脉前降支(LAD)处穿线结扎30 min后,松开结扎线再灌注120min。A、B组在缺血前10 min经股静脉注射生理盐水5 ml·kg-1后以5 ml·kg-1·h-1持续静脉输注至实验结束；布托啡诺组(C组)：缺血前10 min经股静脉注射布托啡诺25μg·kg-1,其它处理同B组；Nor-BNI组(D组)：缺血前20 min经股静脉注射选择性K阿片受体阻断剂Nor-BNI 2 mg·kg-1,余处理同C组；glibenclamide组(E组)：缺血前10 min经股静脉注射KATP通道阻断剂glibenclamide 1 mg·kg1余处理同C组。
实验动物腹腔注射20%乌拉坦1 g·kg-1麻醉后,分离左侧股静脉置入22G套管针,以备输注布托啡诺或生理盐水；连续监测Ⅱ导心电图；气管切开,连接动物呼吸机行机械通气。再灌注结束后,通过股动脉置管收集血样本测定血清TNF-α、IL-6和IL-10的浓度。
结果与假手术组比较,其余各组血清TNF-α、IL-6和IL-10浓度均明显上升(P<0.01)；与缺血/再灌注比较,布托啡诺处理各组血清TNF-α、IL-6浓度降低(P<0.05),IL-10浓度增高(P<0.05)；与布托啡诺组相比,Nor-BNI组和glibenclamide组血清TNF-α、IL-6浓度增高(P<0.05),IL-10浓度降低(P<0.05)
结论布托啡诺可降低大鼠心肌缺血再灌注时促炎性细胞因子的浓度并增加抗炎性细胞因子的浓度,且布托啡诺对这种炎性细胞因子的保护作用部分是通过心肌组织K阿片受体和KATP通道所产生的。
PART 1 Effects of butorphanol tartrate on inflammatory response in septic rats
Objective:To investigate the effects of butorphanol tartrate on inflammatory cytokines in septic rats.
Methods:Forty adult male SD rats weighing 200～250 g were randomly divided into sham-operated group (group C), operated group (group CLP), operated and butorphanol group (group CLP+B) and butorphanol group(group B). Septic shock model was induced by cecal ligation puncture (CLP). Thirty minutes before CLP 5 ml·kg-1 saline and 0.5 mg·kg-1 butorphanol were injected intravenously in group CLP and group CLP+B respectively. Group C and group B only received saline (5 ml·kg-1) and butorphanol (0.5 mg·kg-1) respectively. Mean artery pressure (MAP) and heart rate (HR) were monitored via the right femoral artery. Tumor necrosis factor-α(TNF-α), interleukin-6 (IL-6) and interleukin-10 (IL-10) in serum were measured at 4 h,12 h and 20 h after CLP.
Results:MAP decreased progressively after CLP in group CLP and group CLP+B, while HR increased at first and decreased afterwards in group CLP. The decrease of MAP was inhibited, and the changes of HR were slight in group CLP+B. TNF-α, IL-6 and IL-10 concentrations in group CLP were higher than those in group C at 4,12 and 20 hours after CLP (P<0.05). TNF-a and IL-6 concentrations in group CLP+B were lower than those in group CLP(P<0.05).IL-10 concentrations in group CLP+B were higher than those in group CLP(P<0.05). There were no significant effects on TNF-α、IL-6 and IL-10 concentrations between group C and group B(P>0.05).
Conclusions:Butorphanol tartrate has protective effects on septic shock rats by decreasing pro-inflammatory cytokines TNF-α, IL-6 concentrations and increasing anti-inflammatory cytokine IL-10 concentrations. Butorphanol tartrate has no significant effect on the TNF-α, IL-6 and IL-10 concentrations of normal rats.
PART 2 Effects of butorphanol tartrate on myocardial ischemia reperfusion injury in rats
Objective To observe the effects of butorphanol on myocardial infarct size,malondialdehyde and myocardial structure following myocardial ischemia-reperfusion (I/R) in rats.
Methods Forty healthy male SD rats weighing 200-250 g were randomly divided into five groups with 8 in each group:control group(group A);I/R group(group B); low dosage butorphanol group (group C); moderate dosage butorphanol group(group D) and high dosage butorphanol group(group E). In group B,C,D and E myocardial ischemia-reperfusion was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion.In group C,D and E butorphanol 25μg·kg-1,50μg·kg-1and 100μg·kg-1 was given respectively IV 10 min before occlusion of LAD. The myocardial infarct size was determined by TTC method and the changes of myocardial microstructure were observed under light-microscope. The tissue concentrations of malondialdehyde were measured.
Results The myocardial infarct sizes were both significantly reduced in all butorphanol groups compared with those in I/R group (P<0.05), and myocardial infarct sizes in high dosage butorphanol group were lower than those in low dosage butorphanol group. The myocardial structures of rats in all butorphanol groups were better than those in I/R group, and in moderate dosage butorphanol group and high dosage butorphanol group the myocardial structures were generally normal. Concentrations of malondialdehyde in myocardial ischemia-reperfusion groups were higher than those in control group (P<0.05),Malondialdehyde concentrations in all butorphanol groups were reduced compared with those in I/R group (P<0.05).
Conclusion Butorphanol provide a protective effect on rat heart in a dose-dependent manner following myocardial ischemia-reperfusion.
PART 3 Effects and mechanisms of butorphanol tartrate on inflammatory response in myocardial ischemia-reperfusion rats
Objective To investigate the effect and mechanism of butorphanol tartrate on inflammatory cytokines in myocardial ischemia-reperfusion(I/R) rats.
Methods Forty healthy male SD rats weighing 200～250 g were randomly divided into 5 groups (n=8):control group (group A); I/R group (group B); butorphanol group (group C); Nor-BNI group (group D) and glibenclamide group (group E). In group B,C,D and E myocardial ischemia-reperfusion was produced by occlusion of left anterior descending artery (LAD) for 30 min followed by 120 min reperfusion. In group C,D and E butorphanol 25μg·kg-1 was givenⅣ10min before occlusion of LAD.In group D Nor-BNI 2mg·kg-1 was given IV 20 min before occlusion of LAD.In group E glibenclamide 1 mg·kg-1 was given IV 10 min before occlusion of LAD.In group A and B butorphanol were replaced by normal saline 5 ml·kg-1 followed 5 ml·kg-1-h-1. Blood samples were taken at 120 min of reperfusion for determination of serum TNF-α·IL-6 and IL-10 concentrations.
Result Compared with control group, the concentrations of TNF-a,IL-6 and IL-10 were increased in all myocardial ischemia-reperfusion groups (P <0.01).Compared with I/R group, TNF-αand IL-6 concentrations were decreased and IL-10 concentrations were increased in all butorphanol groups (P<0.05). Compared with butorphanol group, TNF-αand IL-6 concentrations were higher and IL-10 concentration was lower than those in Nor-BNI group and glibenclamide group (P <0.05).
Conclusion Serum TNF-αIL-6 and IL-10 levels were increased following myocardial ischemia reperfusion. Butorphanol decrease pro-inflammatory cytokines TNF-α, IL-6 concentrations and increase anti-inflammatory cytokine IL-10 concentrations. And the effects on cytokines of butorphanol may be attenuated by Nor-BNI or glibenclamide.
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