体外反搏提高切应力调节NO和cGMP机制的探讨

Effects of external counterpulsation on shear stress and production of nitric oxide and cGMP in canines with myocardial infarction

目的观察体外反搏对心肌梗死犬头背干切应力和信号转导物质一氧化氮(NO)和环磷酸鸟苷(cGMP)的影响,探讨体外反搏保护缺血心肌的机制。方法19只健康杂种犬随机分为对照组、缺血组和缺血+反搏组(反搏组)3组,采用开胸结扎冠状动脉左前降支的方法建立心肌缺血模型,观察体外反搏前后头背干切应力的变化,用改良硝酸还原酶法测定体外反搏前后心肌缺血犬血浆和主动脉NO含量,采用放免法检测心肌缺血前后血浆和主动脉cGMP的含量。结果体外反搏可提高因心肌缺血而造成的切应力降低,并使之恢复正常。同时也发现体外反搏可提高缺血组犬血浆和主动脉NO和cGMP水平。结论体外反搏能提高切应力,促进NO和cGMP的产生,这可能是其抗心肌缺血损伤的重要机制之一。

Objective To investigate the effects of external counterpulsation （ECP） on shear stress and signal transduction in canines with myocardial infarction. Methods Nineteen healthy dogs were randomly divided into control, ischemia, and ischemia plus ECP groups. Myocardial infarction was induced in the latter two groups by ligation of the left anterior descending artery （LAD）. Serum and aorta NO levels of the dogs were determined by modified nitrate reductase method, and serum and aorta cyclic guanosine monophosphate （cGMP） levels by radioimmunoassay. Results The shear stress in the truncus brachiocephalicus decreased after LAD ligation, but increased significantly after 2 h of ECP treatment. Serum and aorta NO levels in ECP and control groups were significantly higher than those in the ischemic group （P〈0.05）. Serum and aorta cGMP levels in control group and ECP group after LAD ligation were also significantly higher than those in the ischemic group （P〈0.05）. Conclusion ECP can increase the shear stress and increase NO and cGMP levels in dogs with myocardial ischemia, which might be an imnortant mechanism of ECP for nrotection of the ischemic mvocardium.