Parker J L, Adams H R
Adv Shock Res. 1979;2:163-75.
Atrial myocardium of guinea pigs was used to study effects of Escherichia coli endotoxin shock on inotropic characteristics of heart muscle free from noncardiac influences of the in vivo shock state. In vitro exposure of atrial muscle to large concentrations of endotoxin (10-1,000 microgram/ml, final concentration) for a prolonged period (90 minutes) had no effect on myocardial contractility. However, atrial muscle isolated from endotoxin-shocked guinea pigs exhibited clear evidence of mechanical depression, as reflected by markedly low values for both isometric contractile tension and maximal rate of tension development (dT/dt). Also, since systolic and diastolic time intervals of myocardial contractions were not discernibly affected by shock, the contractile deficit represented a true inotropic dys-function and was not due simply to a temporal change in the active state of the muscle. The shock-induced inotropic disorder was permanent enough to persist in vitro for several hours of observation. However, if the Ca++ concentration of the bathing medium was increased from 2.5 mM to maximally effective concentrations ( greater than 4.5 mM), contractile strength of heart muscle from the shocked group was equal to corresponding responses of control muscles. Present findings verify myocardial contractile dysfunction associated with in vivo endotoxin administration and provide characterization of a test system that should prove useful for further study of functional changes occurring to the heart in shock.
用豚鼠心房肌来研究大肠杆菌内毒素休克对心肌收缩特性的影响，该研究不受体内休克状态下心外因素的影响。将心房肌在体外长时间（90分钟）暴露于高浓度内毒素（最终浓度为10 - 1000微克/毫升）对心肌收缩性无影响。然而，从内毒素休克的豚鼠分离出的心房肌表现出明显的机械抑制迹象，等长收缩张力和张力最大发展速率（dT/dt）的显著低值反映了这一点。此外，由于心肌收缩的收缩期和舒张期时间间隔未受休克明显影响，收缩功能缺陷代表真正的变力功能障碍，并非仅仅由于肌肉活动状态的暂时变化。休克诱导的变力障碍足够持久，在体外观察数小时仍持续存在。然而，如果将灌流液中的Ca++浓度从2.5 mM增加到最大有效浓度（大于4.5 mM），休克组心肌的收缩强度与对照肌肉的相应反应相当。目前的研究结果证实了与体内给予内毒素相关的心肌收缩功能障碍，并提供了一个测试系统的特征描述，该系统应被证明对进一步研究休克时心脏发生的功能变化有用。
