垂体后叶素诱发离体蛙心心肌缺血实验模型

The Myocardial Ischemia Models of Isolated Toad Heart Induced by Pituitrin

目的:建立一个新的心肌缺血实验模型,探讨垂体后叶素对心肌收缩力和心率的直接影响。方法:采用Straub氏法制备离体蟾蜍心脏标本,用任氏液维持心脏的正常活动,加入1ml含有垂体后叶素0.1U/ml的任氏液,记录心肌收缩力和心率的变化。结果:给予垂体后叶素后,心肌收缩力逐渐下降,心率逐渐减慢。在3min时,收缩力由给药前的(4.33±2.30)克降到(0.62±0.48)克(P<0.01),区域时间由(0.52±0.06)秒延迟到(0.64±0.06)秒(P<0.01)。结论:垂体后叶素可以直接抑制心肌收缩,诱发蟾蜍心脏发生心肌缺血。

Objective：To investigate the direct effect of pituitrin on heart contractile in the toad.Methods： Ringers solution was used to maintain the normal action of the heart isolated by the Straub’s method,then the heart was perfused by Ringer’s solution 1 ml containing pituitrin at the concentration of 0.1U/ml,and the myocardiac contractile force and heart rate were recorded separately.Re-sults： It was found that the administrations of pituitrin caused significant decrease of myocardial contractile force and heart rate,com-pared with the controls.Conclusion： The pituitrin has a direct inhibitory effect on the heart and causes heart failure.