创伤失血性休克大鼠血清D-乳酸、二胺氧化酶和内毒素的变化及其对肠黏膜损伤的意义
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摘要
目的探讨创伤失血性休克对大鼠血清D-乳酸、二胺氧化酶和内毒素的水平及其对肠黏膜屏障功能的影响。方法选取成年雄性SD大鼠50只,按照随机数表法将大鼠分为对照组、休克1h组、休克4h组、休克8h组、休克16h组,每组各10只。建立大鼠创伤失血性休克模型后,采用比色法来测定大鼠血清中的二胺氧化酶(DAO)活性;采用光度法来测定大鼠血清中的内毒素、D-乳酸水平。切取大鼠回肠末端组织,观察组织结构病理变化。检测对照组与休克1h组相同时间点采集静脉血液和回肠末端组织。结果各组大鼠静脉血中D-乳酸、二胺氧化酶和内毒素含量组间比较差异有统计学意义(P<0.05)。对照组大鼠肠上皮组织结构完整,无水肿,绒毛无脱落且形态正常。休克1h组肠黏膜组织结构完整,肠绒毛形态不规则;休克4h组部分肠上皮脱落,局部存在水肿,无明显炎细胞浸润;休克8h组上皮组织脱落增多,局部水肿明显,固有层内可见明显炎细胞浸润;休克16h组上皮组织大面积脱落,水肿严重,固有层内炎细胞浸润较8h组更加明显。结论创伤失血性休克早期即发生肠屏障功能障碍,血清D-乳酸、DAO和内毒素是肠黏膜损伤早期诊断的敏感指标,且其水平与肠黏膜组织的病理改变程度呈正相关。
Objective To investigate the effects of traumatic hemorrhagic shock on serum D-lactic acid, diamine oxidase and endotoxin and their effects on intestinal mucosal barrier function in rats. Methods Fifty adult male Sprague-Dawley rats were selected and randomly divided into control group(n=10), 1 h shock group(n=10), 4 h shock group(n=10), 8 h shock group(n=10) and16 h shock group(n=10). After the traumatic hemorrhagic shock model was established in rats, colorimetric assay was used to measure the DAO activity in rat serum. The endotoxin and D-lactic acid levels in rat serum were determined by spectrophotometry. Rat ileum tissue was harvested and the histopathological changes were observed. Venous blood and ileal tissue were collected at the same time points in the control group and the shock 1 h group for detection and observation. Results D-lactic acid, Diamine oxidase and endotoxin levels in each group were statistically different. In the control group, the intestinal epithelium was structurally intact and no villus was absent and the morphology was normal. In the observation group, the intestinal mucosal structure was intact and the intestinal villi were irregular in the 1 h shock group; Part of the intestinal epithelium was shed in the 4 h shock group, with local edema and no obvious inflammatory cell infiltration; The epithelial shedding of the 8 h group was increased, and the local edema was obvious. There was obvious inflammatory cell infiltration in the lamina propria; The epithelial tissue in the 16 h group was severely shedding, and the edema was severe. The infiltration of inflammatory cells in the lamina propria was more obvious than that in the 8 h group. Conclusion In the early stage of traumatic hemorrhagic shock, intestinal barrier dysfunction occurs. Serum D-lactic acid, DAO and endotoxin are sensitive indicators for the early diagnosis of intestinal mucosal injury, and their levels are positively correlated with the pathological changes of intestinal mucosal tissues.
Objective To investigate the effects of traumatic hemorrhagic shock on serum D-lactic acid, diamine oxidase and endotoxin and their effects on intestinal mucosal barrier function in rats. Methods Fifty adult male Sprague-Dawley rats were selected and randomly divided into control group(n=10), 1 h shock group(n=10), 4 h shock group(n=10), 8 h shock group(n=10) and16 h shock group(n=10). After the traumatic hemorrhagic shock model was established in rats, colorimetric assay was used to measure the DAO activity in rat serum. The endotoxin and D-lactic acid levels in rat serum were determined by spectrophotometry. Rat ileum tissue was harvested and the histopathological changes were observed. Venous blood and ileal tissue were collected at the same time points in the control group and the shock 1 h group for detection and observation. Results D-lactic acid, Diamine oxidase and endotoxin levels in each group were statistically different. In the control group, the intestinal epithelium was structurally intact and no villus was absent and the morphology was normal. In the observation group, the intestinal mucosal structure was intact and the intestinal villi were irregular in the 1 h shock group; Part of the intestinal epithelium was shed in the 4 h shock group, with local edema and no obvious inflammatory cell infiltration; The epithelial shedding of the 8 h group was increased, and the local edema was obvious. There was obvious inflammatory cell infiltration in the lamina propria; The epithelial tissue in the 16 h group was severely shedding, and the edema was severe. The infiltration of inflammatory cells in the lamina propria was more obvious than that in the 8 h group. Conclusion In the early stage of traumatic hemorrhagic shock, intestinal barrier dysfunction occurs. Serum D-lactic acid, DAO and endotoxin are sensitive indicators for the early diagnosis of intestinal mucosal injury, and their levels are positively correlated with the pathological changes of intestinal mucosal tissues.
引文
[1] Petroni RC, Biselli PJ, Lima TM, et al. Impact of Time on Fluid Resuscitation with Hypertonic Saline (NaCl 7.5%) in Rats with LPS-Induced Acute Lung Injury[J]. Shock,2015,44(6):609-615.
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[10] 李娟,姜辉,张艳,等.老年危重症患者血浆D-乳酸及内毒素的检测及临床意义[J].胃肠病学和肝病学杂志,2014,23(6):715-717.
[11] 赵永华,杨开敏,贾秀艳,等.丙氨酰谷氨酰胺对重型颅脑损伤患者肠黏膜通透性及血浆二胺氧化酶水平的影响[J].中国全科医学,2014,17(2):214-216.
[12] 汪亨通,项和平,李贺,等.血清二胺氧化酶在重症急性胰腺炎胃肠道功能及病情评估中的作用[J].中华急诊医学杂志,2014,23(12):1381-1384.
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[14] 姚咏明,盛志勇,吴叶,等.大鼠急性肠缺血后D-乳酸的变化及其与肠黏膜损害的关系[J].中国烧伤整形外科杂志,1998,4(4):266-269.
[15] Murdock AD, Berséus O, Hervig T, et al. Whole blood: the future of traumatic hemorrhagic shock resuscitation[J]. Shock,2014,41(1):62-69.
[16] Spahn DR, Bouillon B, Cerny V,et al. Management of bleeding and coagulopathyfollowing major trauma: an updated European guideline[J]. Crit Care,2013,17(2):76.
[17] Thompson JS.The intestinal response to critical illness[J].Am JGastroenterol, 1995,90(2):190-200.
[18] Liu W, Shan LP, Dong XS,et al. Combined early fluid resuscitation and hydrogen inhalation attenuates lung and intestine injury[J]. World J Gastroenterol, 2013,28;19(4):492-502.
[19] 单希胜,詹英.失血性低血容量休克患者早期监测乳酸清除率与休克转归的相关性分析[J].临床麻醉学杂志,2013,29(9):890-891.
[2] Wilmore DW, Smith RJ, O'Dwyer ST,et al. The gut: a central organ after surgical stress[J].Surgery, 1988,104(5):917-923.
[3] Mann V,Mann S,Szalay G,et al.Treatment of polytrauma in the intensive care unit[J]. Anaesthesist, 2010,59(8): 762-763.
[4] 王林林,王兵,于金宝,等.创伤失血性休克大鼠肠系膜淋巴液对血管内皮细胞程序性坏死的影响[J].山东医药,2014,54(8):5-8.
[5] 刘海,赵剑秋,彭晓静,等.内毒素吸附剂SPV对创伤失血性休克模型大鼠肠黏膜损伤的保护作用[J].中国药房,2016,27(10):1333-1336.
[6] 杜舒婷,赵自刚,牛春雨,等.创伤失血性休克血管低反应性发生机制的研究进展[J].中国老年学杂志,2014,34(4):1122-1124.
[7] 张娟娟,王少华,虞文魁,等.猪创伤失血性休克模型凝血功能的变化[J].中华急诊医学杂志,2015,24(5):475-480.
[8] Jeong KY, Suh GJ, Kwon WY, et al. The therapeutic effect and mechanism of niacin on acute lung injury in a rat model of hemorrhagic shock: Down-regulation of the reactive oxygen species-dependent nuclear factor κB pathway[J]. Trauma Acute Care Surg,2015,79(2):247-255.
[9] 刘童蕾,曾玉剑,田衍,等.腹腔间隔室综合征大鼠血浆D-乳酸及二胺氧化酶的变化及意义[J].国际外科学杂志,2016,43(1):23-25.
[10] 李娟,姜辉,张艳,等.老年危重症患者血浆D-乳酸及内毒素的检测及临床意义[J].胃肠病学和肝病学杂志,2014,23(6):715-717.
[11] 赵永华,杨开敏,贾秀艳,等.丙氨酰谷氨酰胺对重型颅脑损伤患者肠黏膜通透性及血浆二胺氧化酶水平的影响[J].中国全科医学,2014,17(2):214-216.
[12] 汪亨通,项和平,李贺,等.血清二胺氧化酶在重症急性胰腺炎胃肠道功能及病情评估中的作用[J].中华急诊医学杂志,2014,23(12):1381-1384.
[13] 侯玥,宫平,杨羽,等.血清二胺氧化酶测定的临床应用进展[J].中国实验诊断学,2015,14(11):1985-1987.
[14] 姚咏明,盛志勇,吴叶,等.大鼠急性肠缺血后D-乳酸的变化及其与肠黏膜损害的关系[J].中国烧伤整形外科杂志,1998,4(4):266-269.
[15] Murdock AD, Berséus O, Hervig T, et al. Whole blood: the future of traumatic hemorrhagic shock resuscitation[J]. Shock,2014,41(1):62-69.
[16] Spahn DR, Bouillon B, Cerny V,et al. Management of bleeding and coagulopathyfollowing major trauma: an updated European guideline[J]. Crit Care,2013,17(2):76.
[17] Thompson JS.The intestinal response to critical illness[J].Am JGastroenterol, 1995,90(2):190-200.
[18] Liu W, Shan LP, Dong XS,et al. Combined early fluid resuscitation and hydrogen inhalation attenuates lung and intestine injury[J]. World J Gastroenterol, 2013,28;19(4):492-502.
[19] 单希胜,詹英.失血性低血容量休克患者早期监测乳酸清除率与休克转归的相关性分析[J].临床麻醉学杂志,2013,29(9):890-891.
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