Changes in heart rate induced by bacterial endotoxin

Publisher Website
Google Scholar
Abstract
In unanesthetized dogs, the intravenous injection of Escherichia coli endotoxin results in an early triphasic change in heart rate; namely, a transient tachycardia, followed by bradycardia, and then a secondary tachycardia. In dogs anesthetized with pentobarbital, there is a similar initial tachycardia, followed by a more prolonged period of bradycardia. When morphine-chloralose-urethan anesthesia is employed, endotoxin also induces an initial tachycardia which is somewhat more prolonged than in the unanesthetized or pentobarbital-anesthetized dogs. Heart rate then returns temporarily to the control level, but accelerates again secondarily. The initial tachycardia observed in all 3 groups of animals is probably ascribable to reduced stimulation of the peripheral baroreceptors by virtue of arterial hypotension. The subsequent bardycardia is due principally to increased neural activity in the cardiac vagal fibers, despite the arterial hypotension. The mechanism has not been determined. In the animals anesthetized with morphine-chloralose-urethan, this tendency for enhanced vagal activity is counteracted by the reflex response to arterial hypotension. When the arterial blood pressure is prevented from falling, then bradycardia appears after endotoxin with this combination of anesthetic agents, just as in the other 2 groups of animals.

This publication has 20 references indexed in Scilit: