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目的：在兔心肌缺血／再灌注前处置模型的基础上，了解NO在心肌缺血前处置中所起的作用及意义。方法：采用免麻醉后开胸结扎左冠状动脉降支，反复结扎（缺血）10分钟，放开（再灌）5分钟，最后结扎30分钟再灌20分钟造成缺血／再灌注前处置模型后，对比观察了各组动物血浆中NO、TXB2、6－K－PGF1α、SOD和MDA浓度的变化，以及各组动物球结膜微循环及心肌病理学的变化。结果：前处置组血浆NO、6－K－PGF1α、SOD浓度显著高于缺血／再灌注组，而MDA、TXB2浓度明显低于缺血／再灌注组。前处置组心肌超微结构损伤明显轻于缺血／再灌注组，球结膜微循环基本正常。结论：心肌缺血前处置可增加心血管内皮细胞合成NO，而NO具有减轻心肌缺血／再灌注损伤、改善微循环障碍的作用。
OBJECTIVE: To investigate the role and significance of nitric oxide in preconditioning of myocardial ischemia on the basis of pre-myocardial ischemia-reperfusion model in rabbits. Methods: Anesthesia-free thoracotomy was performed to ligate left descending coronary artery, ligation (ischemia) for 10 minutes repeatedly, release (reperfusion) for 5 minutes and finally ligation for 30 minutes and then for 20 minutes to cause pre-ischemia / reperfusion model Afterwards, the changes of NO, TXB2, 6-K-PGF1α, SOD and MDA in the plasma of each group were observed and compared, and the changes of conjunctival microcirculation and cardiomyopathies in each group were also observed. Results: The concentration of NO, 6-K-PGF1α and SOD in plasma before treatment were significantly higher than that in ischemia / reperfusion group, while the concentrations of MDA and TXB2 were significantly lower than those in ischemia / reperfusion group. Myocardial ultrastructure damage in the pre-treatment group was significantly lighter than that in the ischemia / reperfusion group, and the conjunctival microcirculation was basically normal. CONCLUSION: Pretreatment with myocardial ischemia can increase the synthesis of NO in cardiovascular endothelial cells, while NO has the effect of reducing myocardial ischemia / reperfusion injury and improving microcirculation.