论文部分内容阅读
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 observe the effect of external counterpulsation (EECP) on the dry back stress and the signal transduction nitric oxide (NO) and cyclic guanosine monophosphate (cGMP) in canine myocardial infarction (AMI) in vitro. Methods Nineteen healthy mongrel dogs were randomly divided into three groups: control group, ischemia group and ischemia + counterpulsation group (EECP group). The model of myocardial ischemia was established by ligating the left anterior descending coronary artery by thoracotomy. Before and after stroke, the changes of head-back dry stress were measured. The contents of NO and NO in plasma and aorta were measured by modified nitrate reductase before and after cardiopulmonary bypass. The contents of cGMP in plasma and aorta were detected by radioimmunoassay. Extracorporeal counterpulsation can increase the shear stress caused by myocardial ischemia and make it return to normal. Also found that extracorporeal counterpulsation can increase plasma and aortic NO and cGMP levels in ischemic dogs. Conclusion Extracorporeal counterpulsation can increase the shear stress and promote the production of NO and cGMP, which may be one of the important mechanisms of anti-ischemic injury.