人urotensinⅡ对大鼠心肌缺血缺氧性损伤的保护作用机制

目的: 探讨人urotensinⅡ(hUⅡ)抗大鼠心肌缺血再灌注损伤的作用机制。方法: 在大鼠冠状动脉左前降支结扎再灌注模型上，观察心电图变化，测定心肌梗死体积及心肌组织中诱导型一氧化氮合酶(inducible NO synthesis, iNOS) mRNA表达。 结果: 0.47、1.4和4.2 μg/kg hUⅡ可明显抑制缺血再灌注损伤大鼠心电图ST段抬高和心肌梗死体积；4.2 μg/kg hUⅡ显著地改善冠状动脉结扎再灌注大鼠心肌细胞超微结构的变化，并增强大鼠心肌组织中iNOS mRNA表达；urotensinⅡ受体（UT）拮抗剂urantide 10 nmol/kg可明显地拮抗1.4和4.2 μg/kg hUII对缺血再灌注大鼠心电图ST段抬高和心肌梗死的抑制作用。结论: HUII抗大鼠心肌缺血性损伤作用可能与激动UT及促进NO合成有关。

Mechanism of human urotensin II on myocardial ischemia-reperfusion injury in rats

AIM: To investigate the mechanism of human urotensin II (hUII) against myocardial ischemia-reperfusion injury in rats. METHODS: On the ligation of anterior decending branch of left coronery artery model, changes of electrocardiogram (ECG) were observed, myocardial infarction volume and inducible nitric oxide synthesis (iNOS) mRNA in myocardial tissue were measured. RESULTS:0.47, 1.4 and 4.2 μg/kg hUⅡ obviously inhibited ECG ST segment elevation and myocardial infarction volume in ischemia-reperfusion injured rats; 4.2 μg/kg hUII significantly improved changes of ultrastructure in myocardial cells and increased the expression of iNOS mRNA in myocardium in rats subjected to myocardial ischemia-reperfusion; UT receptor antagonist urantide (10 nmol/kg) significantly antagonized inhibitory effects of hUII 1.4 and 4.2 μg/kg for ECG ST segment elevation and myocardial infarction. CONCLUSION: Mechanism of hUII against myocardial ischemic injury in rats is related to activation of UT receptor and promotion of nitric oxide production.