Lundgren O, Haglund U, Isaksson O, Abe T
Circ Res. 1976 Apr;38(4):307-15. doi: 10.1161/01.res.38.4.307.
There is a pronounced derangement in cardiovascular function in the cat after a 2- or 3-hour period during which shock is simulated in the small intestine by regional hypotension (BP = 30-35 mm Hg) during activation of vasoconstrictor nerve fibers. It has been proposed that these effects are caused by blood-borne cardiode-pressant substance(s) released from the "shocked" small intestine. To obtain further evidence for this hypothesis we performed a study on two heart preparations in vitro. Rabbit papillary muscles or isolated beating rat hearts were exposed to intestinal venous plasma obtained from control cats and from cats subjected to simulated intestinal shock for 2 or 3 hours. while control plasma induced only a slight depression of myocardial contractility, plasma from "shocked" intestine caused a significant decrease in peak isometric tension of the papillary muscles or a fall in systolic pressure of the rat hearts. Since the experiments on papillary muscle indicated that time to peak tension was largely unaffected by the plasma samples, we conclude that the feline intestine in shock releases material into blood that exerts a negative inotropic effect on the myocardium.
在猫身上，通过在激活血管收缩神经纤维期间使小肠局部低血压（血压 = 30 - 35毫米汞柱）来模拟休克2或3小时后，心血管功能出现明显紊乱。有人提出，这些效应是由“休克”小肠释放的血源性感心抑制物质引起的。为了获得支持这一假设的进一步证据，我们对两个离体心脏标本进行了研究。将兔乳头肌或离体搏动的大鼠心脏暴露于从对照猫以及经历2或3小时模拟肠道休克的猫获取的肠静脉血浆中。对照血浆仅引起心肌收缩力轻微降低，而“休克”肠的血浆导致乳头肌的等长收缩峰值张力显著降低或大鼠心脏的收缩压下降。由于对乳头肌的实验表明达到峰值张力的时间在很大程度上不受血浆样本的影响，我们得出结论，休克状态下的猫小肠会向血液中释放对心肌产生负性肌力作用的物质。
