等容血液稀释和川芎嗪对兔心肌缺血再灌注损伤的保护作用

来源 :中华麻醉学杂志 | 被引量 : 0次 | 上传用户:lijb2009
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目的 观察6%羟乙基淀粉(HAES)等客血液稀释和川芎嗪注射液对兔心肌缺血再灌注损伤的保护作用。方法 32只家兔随机分为4组(n=8):组Ⅰ(对照组);组Ⅱ(稀释组);组Ⅲ(川芎嗪组);组Ⅳ(稀释+川芎嗪组),观察在急性心肌缺血45min和再灌注180min状态下血浆及心肌组织中磷酸肌酸激酶(CPK)及乳酸脱氢酶(LDH)活性的变化,并以透射电镜观察心肌超微结构改变。结果缺血及再灌后,组Ⅰ血浆CPK、LDH活性进行性升高(P<0.05,P<0.01),缺血区心肌组织CPK、LDH活性明显降低(P<0.01)。再灌后与组Ⅰ相比,组Ⅱ、Ⅲ血浆LDH活性均降低(P<0.05),组Ⅱ缺血区心肌组织CPK、LDH活性均升高(P<0.05),组Ⅲ缺血区心肌组织CPK活性升高(P<0.05),组Ⅳ血浆CPK、LDH活性均降低(P<0.05,P<0.01),且LDH活性低于同期组Ⅱ(P<0.05),缺血区心肌组织CPK、LDH活性均显著升高(P<0.01),且CPK活性高于组Ⅲ缺血区(P<0.05)。心肌细胞超微结构可见组Ⅰ细胞结构破坏严重,组Ⅱ、Ⅲ结构破坏均较组Ⅰ轻,组Ⅳ结构基本接近正常。结论 6%HAES等容血液稀释和川芎嗪对心肌缺血再灌注损伤均有保护作用,二者合用保护作用更为显著。 Objective To observe the protective effects of hemodilution such as 6% hydroxyethyl starch (HAES) and ligustrazine injection on myocardial ischemia-reperfusion injury in rabbits. Methods Thirty-two rabbits were randomly divided into 4 groups (n=8): Group I (control group); Group II (dilution group); Group III (Tetramethylpyrazine group); Group IV (dilution + Ligustrazine group). The changes of phosphocreatine kinase (CPK) and lactate dehydrogenase (LDH) activity in plasma and myocardial tissue were observed under the conditions of 45 minutes of acute myocardial ischemia and 180 minutes of reperfusion, and ultrastructural changes of myocardium were observed under transmission electron microscope. Results After ischemia and reperfusion, the activity of CPK and LDH in plasma of group I was increased (P<0.05, P<0.01), and the activity of CPK and LDH in myocardial tissue of ischemic region was significantly decreased (P<0.01). After reperfusion, compared with group I, the activity of plasma LDH in group II and III was decreased (P<0.05). The activity of CPK and LDH in myocardial tissue of group II was increased in group II (P<0.05). Group III myocardial ischemic area The activity of CPK was increased (P<0.05). The activities of CPK and LDH in group IV plasma were all decreased (P<0.05, P<0.01), and LDH activity was lower than that in group II (P<0.05). Myocardial tissue CPK in ischemic region LDH activity was significantly increased (P<0.01), and CPK activity was higher than that of Group III ischemic area (P<0.05). Myocardial ultrastructure showed that the cell structure of I was severely damaged, and the structural damage of group II and III was lighter than that of group I. The structure of group IV was almost normal. Conclusion The 6% HAES isovolumic hemodilution and ligustrazine all have protective effects on myocardial ischemia-reperfusion injury, and the combined protective effect is more significant.
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