应激大鼠血浆同型半胱氨酸水平的变化及其对心功能的影响

目的观察应激对大鼠血浆皮质酮和同型半胱氨酸（homocysteine,HCY）水平的影响及其与心功能变化的关系。方法用雄性Wistar大鼠，采用束缚应激法建立应激动物实验模型，八导生理记录仪监测应激前后大鼠心电图的改变。分别采用放射性免疫法和高压液相荧光检测法测定血浆皮质酮、HCY浓度。分离培养Wistar乳鼠心肌细胞，以台盼蓝排斥实验检测HCY对细胞存活率的影响。结果应激后大鼠血浆HCY、皮质酮的浓度均明显提高，其中应激即刻HCY升高227.1%，皮质酮升高704.2%；慢性应激使心电图发生传导阻滞、心肌缺血、心肌梗死等的特征性变化，心功能发生不可逆损伤；应激后HCY血浆浓度的改变与心电图异常发生率关系密切；HCY对心肌细胞存活率的影响有明显的量效和时效关系，1×10－3mol/LHCY作用于心肌细胞48小时后使存活率降至30.7%。结论除遗传性诱因和营养性诱因外，应激是引起血浆HCY水平升高的又一因素；HCY可能介入应激引起的心功能紊乱；该效应的发生与HCY的心肌细胞损伤作用有关。

Change of homocysteine level in plasma of stressed rats and its effect on cardiac function

Objective:To study the influence of stress on homocysteine(HCY) and corticosterone content in plasma of rats and its effect on cardiac function following these changes.Methods:Experiments were performed on male Wistar rats.The concentration of HCY and corticosterone in plasma were determined by high pressure liquid chromatography(HPLC)fluorometry and radioimmunoassay respectively after acute and chronic restrain stress.And the eightchannel physiological recorder was used to monitor electrocardiogram(ECG)of rats once a week.Primary cardiomyocyte from neonatal rats were exposed to different HCY levels for 12,24 or 48 hours.Cell injury was evaluated using Trypan Blue stained assay.Results:The level of corticosterone and HCY increased significantly owing to stress.Thereinto after acute stress,the concentration of corticosterone and HCY were increased 704.2% and 227.1% respectively(P<0.05 or P<0.01).Irreversible changes of ECG came of chronic stress,and these changes purport myocardial ischemia,myocardial infarction,and so on.Exposure of cardiomyocytes to HCY induced markedly cell injury in concentration and timedependent manner (decrease of viability to 30.7% under the condition of 1×10－3 mol/L HCY for 48 hours).Conclusions:Stress is an important factor for increasing concentration of HCY except for the two wellknown genetic and nutritional inducement.The parallel trend between the increase in HCY content and the abnormal ECG suggests that HCY involves in the stress injury of cardiac function.The cardiomyocyte injury by HCY may contribute to the cardiac dysfunction.