Effects of blockade of vasopressin V-1 receptors on post-burn myocardial depression

Abstract

It has been suggested that post-burn myocardial depression may be due to coronary constriction which results in myocardial ischaemia. It has been demonstrated that the levels of vasopressin, a potent natural constrictor of blood vessels, increase four-to six-fold immediately after thermal trauma. Therefore, this substances could be responsible for post-burn coronary constriction and myocardial depression. This was tested using the dog anaesthetized with sodium pentobarbital receiving a 15 per cent total body surface area full thickness, flame burn as the experimental model. Cardiac output was measured by the thermal dilution technique. Arterial blood pressure was sensed by a Stathem P-23 transducer. Cardiac force of contraction was measured by a Walton-Brody strain gauge arch sewn on the left ventricle. The results of this study showed a significant decrease in cardiac output, increase in peripheral resistance and decrease in myocardial force of contraction immediately after thermal trauma in untreated animals. The decrease in cardiac output and increase in peripheral resistance remained for the duration of the experimental observations (3 h). The decrease in force of contraction returned to preburn levels in post-burn. Pretreatment of the experimental animals with d(CH 2) s Tyr(Me)AVP (SK&F 100273), a vasopressin, V-I receptor blocking agent, prevented the initial decrease in cardiac output, increase in peripheral resistance and decrease in the force of contraction. A correlation plot of peripheral resistance vs. cardiac force of contraction showed a positive correlation between these two variables in the pretreated animals. These results suggest that vasopressin plays an important role in the initial decrease in force of contraction and that coronary constriction may be responsible for the post-burn depression of myocardial force of contraction.