心肌缺血再灌注时氧化亚氮与氧化亚氮合酶的变化及L-精氨酸对其的影响

目的：观察大鼠心肌缺血再灌注时氧化亚氮（nitric oxide，NO）和氧化亚氮合酶（nitric oxide synthase，NOS）的变化及L-精氨酸对其的影响，探讨心肌缺血再灌注损伤的可能机制。方法：大鼠80只，分为假手术对照（sham）组，心肌缺血再灌注组，肾脏缺血预处理＋心肌缺血再灌注组和L-精氨酸治疗＋心肌缺血再灌注组，检测血清NO及NOS水平，光镜下进行中性粒细胞计数。结果：缺血再灌注（MIR）组缺血30min时相点与对照组相比NO，NOS无差异，再灌注后NO，NOS开始下降，随时间延长，NO，NOS逐渐减少。与MIR组再灌注对应时相比较，肾脏缺血预处理＋MIR组及精氨酸治疗＋MIR组NO及NOS均显著增加。缺血后再灌注时随时间延长，中性粒细胞数量逐渐增加，给予精氨酸干预或肾脏缺血预处理后中性粒细胞数量显著下降。结论：心肌缺血后再灌注时有大量中性粒细胞浸润，与心肌损伤关系密切。缺血预处理可通过增加NO水平减轻随后的缺血再灌注损伤，L-精氨酸可通过增加NO，减少中性粒细胞浸润起心肌保护作用。

Changes of NO and NOS in Myocardial Ischemic Reperfusion and Effects of L-Arginine

Objective: To observe the changes of nitric oxide and nitric oxide synthase in ischemic-reperfused myocardium,to observe the effects of L-Arginine on the changes of nitric oxide and nitric oxide synthase,and to investigate the mechanism of myocardial ischemic-reperfusion injure.Methods: Eighty rats were divided into four groups: Sham-group,MIR+RIP group,MIR group and L-Arginine+MIR group.The last three groups received post-ischemic30 minutes,reperfusion for 30min,60mim,120min and 240min.The changes of serum nitric oxide and nitric oxide synthase were examined.The numbers of PMNs in cardiac tissue were counted.Results: No difference was found between sham group and MIR group at 30 minutes after ischemia.The levels of nitric oxide and nitric oxide synthase were decreased significantly after reperfusion.Compared with MIR groups,the levels of nitric oxide and nitric oxide synthase were increased significantly in MIR+RIP group and L-Arginine+MIR group.The numbers of PMNs were significantly increased in ischemic-reperfused myocardium. The numbers of PMNs were significantly decreased in ischemic-reperfused myocardium after giving L-Arginine or ischemic preconditioning.Conclusion: The myocardial neutrophil infiltration indicated that the neutrophils participated in impairing the myocardium during myocardial ischemic reperfusion.Ischemic preconditioning can relieve the heart ischemic reperfusion injury by the increasing levels of the nitric oxide.L-Arginine prevented the neutrophils filtration from myocardial infiltration,and ameliorated the ischemic reperfusion injury by the increasing levels of the nitric oxide.