Site of action of endotoxin in evoking bradycardia

Abstract

Previous investigation of the mechanism responsible for the bradycardia evoked by the intravenous injection of bacterial endotoxin revealed that the primary site of action of the endotoxin must be some subdiaphragmatic structure. The present study was undertaken to localize more precisely this site of action. In anesthetized dogs, the renal pedicles or the intestinal arteries were ligated before endotoxin was administered. It was found that exclusion of the intestinal vascular bed prevented the fall in heart rate, whereas occlusion of the renal vasculature did not alter the cardiac response. To localize the mesenteric site of action of endotoxin more precisely, small doses of endotoxin were injected into each of the individual intestinal arteries and into the splenic artery and the portal vein. The response was compared with that evoked by the injection of an equivalent amount of endotoxin into a femoral artery. It was observed that when endotoxin was injected into the intestinal arteries, bradycardia resulted. However, when endotoxin was injected into the femoral artery or the portal vein, no significant change in heart rate was detected, indicating that the intestines probably are the site of action for evoking bradycardia.