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目的:探讨氯胺酮对大鼠实验性心肌缺血再灌注时心肌细胞凋亡与Fas及Fas蛋白配体(FasLi-gand,FasL)表达的影响,并分析心肌组织病理学损伤程度。方法:以穿线结扎或松扎左冠状动脉制备大鼠心肌缺血再灌注模型。32只大鼠随机平均分成假手术组(假手术4.5 h)、缺血再灌注组(缺血30min、再灌注4 h)、低剂量氯胺酮再灌注组(缺血30 min、再灌注4 h)及高剂量氯胺酮再灌注组(缺血30 min、再灌注4 h)。以缺口末端标记法检测心肌细胞凋亡的变化,S-P免疫组化法分别检测Fas与FasL蛋白水平变化,做病理组织切片检查心肌损伤情况。结果:心肌缺血再灌注前心肌细胞凋亡指数、Fas蛋白阳性染色指数与炎性细胞FasL蛋白阳性染色指数分别为4.25±2.04、1.06±0.25和0,心肌缺血再灌注后心肌细胞凋亡指数、Fas蛋白阳性染色指数和炎性细胞FasL蛋白阳性染色指数分别为12.58±1.35,11.05±3.02和8.12±3.54,低剂量氯氨酮作用组心肌细胞凋亡指数及Fas蛋白阳性染色指数与炎性细胞FasL蛋白阳性染色指数分别为7.36±1.30,7.61±3.41和3.69±3.13;心肌缺血再灌注后心肌组织呈大小不一的灶性坏死,坏死周围有炎性细胞浸润,氯胺酮作用后坏死减轻,低剂量氯胺酮作用更明显。结论:心肌缺血再灌注时心肌细胞凋亡、Fas基因的蛋白与炎性细胞的FasL蛋白表达量均增加,氯氨酮可减少心肌凋亡,减少细胞Fas和FasL蛋白阳性表达,从而减轻心肌损伤,且低剂量氯氨酮作用更明显。
Objective: To investigate the effects of ketamine on the apoptosis of cardiomyocytes and the expression of Fas and Fas ligand in experimental myocardial ischemia / reperfusion in rats, and to analyze the degree of myocardial histopathology injury. Methods: Myocardial ischemia - reperfusion model was made by ligating the ligament or loosening the left coronary artery. Thirty-two rats were randomly divided into sham operation group (sham operation 4.5 h), ischemia reperfusion group (ischemia 30 min, reperfusion 4 h), low dose ketamine reperfusion group (ischemia 30 min, reperfusion 4 h) And high-dose ketamine reperfusion group (ischemia 30 min, reperfusion 4 h). The changes of myocardial apoptosis were detected by nick end labeling. The changes of Fas and FasL protein levels were detected by S-P immunohistochemistry, and the myocardial injury was examined by histopathological examination. Results: The myocardial apoptosis index, Fas protein positive staining index and inflammatory cell FasL protein positive staining index were 4.25 ± 2.04, 1.06 ± 0.25 and 0 respectively. The myocardial apoptosis after myocardial ischemia / reperfusion Index, positive staining index of Fas protein and positive staining index of FasL protein in inflammatory cells were 12.58 ± 1.35, 11.05 ± 3.02 and 8.12 ± 3.54 respectively. Apoptosis index and Fas protein positive staining index and inflammation in low dose ketamine group The positive staining index of FasL protein was 7.36 ± 1.30, 7.61 ± 3.41 and 3.69 ± 3.13, respectively. Myocardial tissue showed myocardial necrosis with different sizes after myocardial ischemia and reperfusion, with infiltration of inflammatory cells around the necrosis and necrosis after ketamine treatment Reduce the role of low-dose ketamine more obvious. CONCLUSION: Myocardial apoptosis, the expression of Fas gene and FasL protein in inflammatory cells are increased during myocardial ischemia-reperfusion. Ketamine can reduce myocardial apoptosis, decrease the expression of Fas and FasL protein, Injury, and the role of low-dose ketamine more obvious.