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目的 :探讨一氧化氮 (NO)和内皮素 (ET)在心肌缺血再灌注损伤 (MIRI)中的作用及川芎嗪对其的影响。方法 :实验兔分为假手术对照组 (n =10 )、心肌缺血再灌注组 (n =10 )及心肌缺血再灌注 +川芎嗪组 (n =10 ) ;分别检测缺血前、缺血 40min和再灌注 2 0min 3个时点的指标变化。检测血浆及心肌组织一氧化氮代谢产物 (NOP)含量、测定ET水平、乳酸脱氢酶 (LDH)活性 ,并行心肌电镜观察。结果 :心肌缺血 40min、再灌注 2 0min血浆NOP明显低于、ET及LDH显著高于假手术对照组 ,尤以再灌注 2 0min变化显著 (均P <0 0 1) ;心肌组织NOP和LDH明显低于、ET显著高于假手术对照组 (P <0 .0 5和P <0 .0 1) ;心肌超微结构发生异常改变。川芎嗪可逆转上述指标的异常变化。结论 :缺血再灌注导致血管内皮功能紊乱 (即NO水平下降和ET水平升高 ) ,在MIRI发生发展中起介导作用 ;川芎嗪通过保护冠脉内皮 ,提高机体内NO水平和降低机体内ET水平 ,从而减轻MIRI
Objective: To investigate the role of nitric oxide (NO) and endothelin (ET) in myocardial ischemia-reperfusion injury (MIRI) and the effect of ligustrazine on them. Methods: Experimental rabbits were divided into sham operation group (n = 10), myocardial ischemia-reperfusion group (n = 10) and myocardial ischemia-reperfusion group and ligustrazine group (n = 10) Blood 40min and reperfusion 20min 3:00 point changes. The content of nitric oxide metabolites (NOP) in plasma and myocardium was detected. The level of ET and the activity of lactate dehydrogenase (LDH) were measured and observed by myocardial electrocardiography. Results: The NOP and LDH levels in myocardial ischemia 40 min and 20 min after reperfusion were significantly higher than those in sham-operation control group, especially at 20 min reperfusion (all P <0.01); NOP and LDH Significantly lower than that of the control group, ET was significantly higher than the sham-operated control group (P <0.05 and P <0.01); myocardial ultrastructure was abnormally changed. Ligustrazine can reverse the abnormal changes in the above indicators. CONCLUSION: Ischemia / reperfusion leads to endothelial dysfunction (ie, decreased NO level and increased ET level) and plays a mediating role in the development and progression of MIRI. Ligustrazine can protect the coronary endothelium and increase the level of NO in the body, ET level, thereby reducing MIRI