Senges J, Mizutani T, Pelzer D, Brachmann J, Hennig E, Mehmel H C, Mäurer W, Wieland H, Katus H, Kübler W
Basic Res Cardiol. 1978 Mar-Apr;73(2):147-59. doi: 10.1007/BF01906750.
The inotropic and electrophysiological effects of plasma obtained from patients and experimental dogs during cardiogenic shock following acute myocardial infarction were studied. Changes in the isometric contraction and the intracellular action potential were determined in isolated papillary muscles of rabbits. Control plasma collected from normal subjects produced no significant changes in the contraction or the electrical parameters. Plasma from shock patients decreased peak force by 42% and the maximum rate of force development by 38% in comparison to control values; the time to peak of contraction, the relaxation time and the action potential parameters were not significantly altered. Corresponding results were obtained with plasma from dogs before and during experimental cardiogenic shock. Biochemical determinations failed to identify a single specific "myocardial depressant factor" in the plasma of patients and dogs with cardiogenic shock. The results suggest that (1) various humoral factors released during cardiogenic shock may depress the contractile function of cardiac muscle and (2) that the observed negative intropic effect is not due to electrical changes in the cell membrane.
对急性心肌梗死后心源性休克患者及实验犬的血浆进行了变力性和电生理效应研究。测定了兔离体乳头肌等长收缩和细胞内动作电位的变化。从正常受试者采集的对照血浆对收缩或电参数无显著影响。与对照值相比,休克患者的血浆使峰值力降低了42%,最大力发展速率降低了38%;收缩达峰时间、舒张时间和动作电位参数无显著改变。实验性心源性休克前后犬的血浆也得到了相应结果。生化测定未能在患有心源性休克的患者和犬的血浆中鉴定出单一特定的“心肌抑制因子”。结果表明:(1)心源性休克期间释放的各种体液因子可能会抑制心肌的收缩功能;(2)观察到的负性变力作用并非由于细胞膜电变化所致。