Extrahepatic factors in the early hypotensive response to bacterial endotoxin

Abstract

Experiments were designed to determine the relative importance of hepatic and extrahepatic factors in the arterial hypotension observed shortly after the injection of bacterial endotoxin. In one series of experiments, the increase in portal venous pressure, ordinarily evoked by endotoxin, was markedly attenuated by means of a servo-controlled pump. Despite the absence of an appreciable rise in portal venous pressure, arterial pressure progressively fell 50 mm Hg, below the control level, during the first 30 min after endotoxin. In a second series of experiments, a comparison was made between dogs in which the hepatic circulation was either bypassed or included in the circulation. With the liver excluded, arterial pressure declined 40 mm Hg, below control, in the first 15 min after endotoxin. The fall in arterial pressure in both series is believed to be attributable to venous pooling in regions other than the hepatoportal vascular bed.