Why the study?
Does intestinal venous plasma from cats in simulated shock reduce myocardial contractility in isolated heart preparations?
Does intestinal venous plasma from cats in simulated shock reduce myocardial contractility in isolated heart preparations?
The feline intestine in simulated shock releases blood-borne material that exerts a negative inotropic effect on the myocardium in vitro.
May implicate intestinal factors in shock-related myocardial depression; leaves open relevance to human cardiogenic shock and needs in vivo validation.
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.
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Lundgren et al. (1976) studied this question.
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