抑制诱生型一氧化氮合酶对大鼠心肌梗死后左心室形态及心功能的影响

目的 :探讨抑制诱生型一氧化氮合酶 (iNOS)对大鼠心肌梗死后左心室形态及心功能的影响。方法 :结扎大鼠左冠状动脉建立心肌梗死模型。免疫组化检测心肌iNOS表达水平。分别于心肌梗死发生前、心肌梗死 7d后开始iNOS抑制剂S methylisothiourea (SMT)干预 ,于心肌梗死 6周后测定血浆一氧化氮 (NO)、心肌iNOS表达、左心室形态变化和心功能。结果 :心肌梗死 6周后心肌iNOS表达增加 ,血浆NO水平上升。于心肌梗死发生前、心肌梗死 7d后开始SMT干预均可降低血浆NO水平 ,减轻心室扩张 ,减轻心室重量 ,改善心功能。心肌梗死发生前开始SMT干预尚可提高存活率。结论 :iNOS在心肌梗死后心功能障碍的发生发展过程中起促进作用 ,抑制iNOS可以改善左心室功能 ,其机制与减轻心肌梗死后左心室重构有关。

Effect of iNOS inhibiting on left ventricular morphologic and haemodynamic parameters after myocardial infarction

Objective:To characterize the effects of an iNOS inhibitor, S-methylisothiourea (SMT)on left ventricular morphological and heamodynamic parameters after myocardial infarction.Method:Myocardial infarction (MI) was induced by ligation of left coronary artery in rats. Animals were assigned to sham, MI , SMT1 (SMT intervention beginning at 30 min before MI), or SMT2 (SMT intervention beginning at 7 d after MI) groups. Left ventricular morphological studies and heamodynamic studies were performed at 6 week after MI. Result:Six weeks after MI, iNOS level in myocardium was elevated, accompanied by increased plasma NO level. Intervention by SMT could decrease plasma NO level, LV circumference, inner LV diameter, and improve cardiac function in two SMT groups. Conclusion:iNOS was involved in the development of cardiac dysfunction after MI. Inhibition of iNOS could exert beneficial effects on cardiac remodelling processes and heart dysfunction.