失血性休克条件下心肌细胞动作电位和心肌力学的改变的研究

Myocardial Cells Action Potential and Contractive Function in Hemorrhagic Shock in Rabbits

家兔失血性休克低血压5．3KPa观察3h，测定平均动脉压（MBP）、左心室收缩压（LVSP）、左心室最大收缩速度（dp／dtmax）以及心肌细胞电生理和组织内外钾钠。结果说明：（1）失血性休克后LVSP下降，且和MBP平行，（2）dp／dtmax在失血性休克后即刻急剧下降，15min后上升48％，以后逐渐下降，3h降至对照值的20％；（3）休克时细胞外钾钠显著升高；（4）心肌细胞静息电位（RP）、动作电位振幅（APH）下降；动作电位复极时间（APD），动作电位复极50％时间（APD50），复极90％时间（APD90）显著延长。提示；心肌细胞快钠通道关闭、慢钠和慢钙通道开放，钠、钙内流，钾外流。

Anesthetized rabbits were subjected to a moderate degree of hemorrhagic shock. Lowering theirmean arterial pressure to 5. 3 KPa for 3 h, we measured the mean arterial pressure (MBP), left ventricular systolicpressure (LVSP), left ventricular maximum velocities of contraction (dp/dtmax), and myocardial electrical activity.The results of this study demonstrated that LVSP declined in parallel with MBP I that dp/dtmax dropped acutely on the instant of hemorrhagic shock ; dp/dtmax went up by 48N on 15 min after shock ; then dp/dtmax fell gradully, and by 3 h after shock the dp/dtamx values dropped to 20% of the baseline values ; that intracellular sodium andpotassium contents increased significantly in the hemorrhagic shocked rabbits; that myocardial resting potential(RP) and action potential amplitude (APH) diminished ; and that action potential duration(APD), action potentialrepolarized 50% duration (APD 50), and repolarized 90% duration (APD 90) were markedly prolonged in thehemorrhagic shock, compared with control. The results suggested that in hemorrhagic shock myocardial cells fastsodium channel was closed while slow sodium and slow calcium channels, were opened ; thus sodium and calciuminfused and potassium exuded.