Circulatory response to bilateral common carotid artery occlusion in hemorrhagic shock

Abstract

Although numerous reports have been published on the carotid sinus reflex, only a few have dealt specifically with the activity of this reflex in acute hemorrhagic hypotension. The purpose of the reported experiments was to study the carotid sinus reflex in reversible and irreversible stages of hemorrhagic shock. Methods In 23 dogs anesthetized with alpha-chloralose and bilaterally vagotomized or atropinized, hemorrhagic irreversible shock was induced by arterial bleeding to a mean blood pressure of 48mmHg. This pressure was maintained for 4 hours, after which the bled volume was reinfused. Changes in arterial blood pressure, carotid sinus pressure, right intraventricular pressure, cardiac output and total peripheral resistance (TPR) were measured before and during bilateral common carotid occlusion. Continuous recordings of these changes were made in a control period and every two hours during a period of hemorrhagic hypotension. Hemodynamic changes produced by carotid occlusion were also studied 10 minutes after blood reinfusion and thereafter every 30 minutes until the animal expired. Three experiments were performed on chloralosed dogs that were subjected to short periods (5 to 30 minutes) of hemorrhagic hypotension. Results In the control period, occlusion of the common carotid arteries gave rise to an increase in arterial pressure, heart rate, right intraventricular pressure and TPR, while cardiac output remained at the preocclusive level. During the 4 hour period of hypotension, carotid occlusion gave rise to an elevation in blood pressure and TPR, while heart rate and intraventricular pressure did not change. Regardless of the stage of shock studied, carotid occlusion did not cause cardiac output to change significantly. Ten minutes after the infusion of blood, occlusion caused an increase in blood pressure and TPR which, despite the return of blood pressure to near control levels, was not as significant as that observed during the control. In the irreversible state of shock following blood rein-fusion, subsequent bouts of carotid occlusion elicited increases in blood pressure and TPR that were found to be less in magnitude than those observed during the hypotension period. In three dogs subjected to short periods of acute hemorrhagic hypotension, TPR responses to carotid occlusion were found to be far greater at the same preocclusive blood levels than of those animals in irreversible hemorrhagic shock.