延髓腹外侧一氧化氮介导电针内关对急性心肌缺血大鼠心功能的作用

实验在以乌拉坦和氯醛糖混合麻醉的雄性SD大鼠上进行。结扎左冠状动脉前降支以建立急性心肌缺血(AMI)动物模型。病理学检查显示该模型具有典型的心肌缺血改变。功能学改变包括心率(HR)减慢、平均动脉压(MAP)降低,以及心功能减弱,如左室舒张末压(LVEDP)增大,左室收缩压(LVSP)、左室压变化最大速率(±dp/dt)、左室收缩成分缩短速度(VCE)、心力环总面积(L0)等均明显减小。电针AMI大鼠的内关穴位20 min,可使其HR、MAP、LVEDP、LVSP、±dp/dt、VCE和L0等均明显改善。若电针前于延髓头端腹外侧区(RVLM)微量注射一氧化氮合酶(NOS)抑制剂L-NNA(0.1 mmol/L,0.1 μl),除HR和MAP外,电针改善AMI心功能的其余各项指标均减弱或被取消,而以等量的生理盐水取代L-NNA被注入RVLM时,则不能影响EA对AMI各项心功能指标的改善作用。以上结果提示电针内关改善AMI的作用由RVLM的一氧化氮(NO)所介导。

Medullary ventrolateral nitric oxide mediates the cardiac effect of electroacupuncture at "Neiguan" acupoint on acute myocardial ischemia in rats

Experiments were performed on male Sprague-Dawley (SD) rats anesthetized with a mixture of urethane and chloralose. A rat model of acute myocardial ischemia (AMI) was made by ligation of the left anterior descending branch of the coronary artery (LAD). After the LAD ligation, the ischemia area of the left ventricular wall became somewhat pale immediately. Under a light microscope, the pathological examination revealed that all the cells were swollen and in red color when the cardiac section was stained with hematoxylin basic fuchsin picric acid (HBFP), which indicated a typical change in the myocardial ischemia. In the AMI model, it was found that cardiac functions were markedly attenuated, such as decreases in the heart rate (HR), mean arterial pressure (MAP), left ventricular systolic pressure (LVSP), maximal rate for left ventricular pressure rising and declining (+/-dp/dt(max)), velocity of contractile element (V(CE)) and total area of cardiac force loop (L(0)), and an increase in the left ventricular end diastolic pressure (LVEDP). In such AMI rats, application of electroacupuncture (EA) at "Neiguan" acupoints (Pe 6) for 20 min could obviously improve the above-mentioned cardiac functions. After microinjection of nitro-L-arginine (L-NNA), an inhibitor of nitric oxide synthase (NOS), was made into the rostral ventrolateral medulla (RVLM), the curative effect of EA on myocardial ischemia was reduced significantly or abolished, while after microinjection of normal saline of the same volume was made into the RVLM, the improving effect of EA remained. These results suggest that the effect of EA on myocardial ischemia is possibly mediated by the nitric oxide (NO) in the RVLM.