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目的:研究心肌缺血再灌注与心肌缺血后处理两种因素下大鼠心肌一氧化氮(NO)的含量与一氧化氮合酶(niricoxide syn-thase,NOS)活性的关系。方法:采用健康雄性Wistar大鼠(n=12)建立离体心肌缺血再灌注损伤模型。采用高效液相色谱仪(HPLC)直接测定心脏灌流液中NO的含量。采用高效液相色谱仪(HPLC)测定瓜氨酸生成量计算心肌中NOS活性。使用紫外分光光度法测定乳酸脱氢酶(LDH)活性。使用染色法计算心肌梗死面积。结果:平衡末,对照组NO含量与实验组NO含量差异无统计学意义(P>0.05);对照组平衡末NO含量与再灌注后NO含量差异无统计学意义(P>0.05);对照组再灌注后NO含量与实验组后处理后NO含量相比差异有统计学意义(P<0.05);实验组后处理后NO含量与平衡末NO含量相比显著升高(P<0.05)。实验组后处理后心肌组织NOS活性明显高于对照组(P<0.05)。实验组心肌释放的LDH活性显著低于对照组(P<0.01)。与对照组比较,缺血后处理可减少心肌梗死面积(P<0.05)。结论:缺血后处理时心肌细胞中NO生成量与NOS活性普遍高于缺血再灌注时。
Objective: To study the relationship between the content of nitric oxide (NO) in myocardium and the activity of niricoxide syn-thase (NOS) in rats with myocardial ischemia-reperfusion and myocardial ischemic postconditioning. Methods: A model of isolated myocardial ischemia-reperfusion injury was established in healthy male Wistar rats (n = 12). The content of NO in cardiac perfusate was determined directly by high performance liquid chromatography (HPLC). NOS activity in myocardium was calculated by measuring the amount of citrulline produced by high performance liquid chromatography (HPLC). Determination of lactate dehydrogenase (LDH) activity using UV spectrophotometry. The area of myocardial infarction was calculated using staining. Results: At the end of balance, there was no significant difference between NO content in control group and NO in experimental group (P> 0.05). There was no significant difference in NO content between control group and NO after reperfusion (P> 0.05) The content of NO after reperfusion was significantly lower than that of experimental group after treatment (P <0.05). The content of NO in experimental group was significantly higher than that at the end of equilibrium (P <0.05). The NOS activity of myocardium in the experimental group was significantly higher than that in the control group (P <0.05). LDH activity in experimental group was significantly lower than that in control group (P <0.01). Compared with the control group, ischemic postconditioning could reduce the area of myocardial infarction (P <0.05). CONCLUSION: NO production and NOS activity in myocardial cells during ischemic postconditioning are generally higher than those during ischemia / reperfusion.