Haemorrhage-induced splenic vasodilation in the rat is mediated by sympathetic vasomotor nerves.

Abstract

A marked decrease in splenic vascular resistance, with an increase in blood flow to the spleen, occurs already 5 min after an acute and severe hypotensive bleeding in awake rats. This response is virtually abolished in rats pretreated with a beta-adrenergic blocking agent. We have now studied the contribution of the sympathetic vasomotor innervation and of adrenal gland-derived catecholamines to the splenic vasodilation. Splenic blood flow was determined with the microsphere method in heavily bled (1.5% of body weight) awake rats. The sympathetic neurones in one group of rats had been chemically destroyed with 6-hydroxydopamine. In another group of rats we had removed the adrenal glands. In the control and in sympathectomized rats, splenic vascular resistance fell to 35 and 64%, respectively, of baseline 5 min after bleeding. Splenic blood flow about doubled during this period in the control rats, and then declined gradually to baseline over the next 24 h. In the sympathectomized rats, splenic blood flow decreased gradually over the first 12 h to reach 66% of baseline. The removal of the adrenal glands did not appreciably influence the splenic vascular response to bleeding. We conclude that an increased activity in the splenic sympathetic vasomotor neurones is a prerequisite for the observed vasodilation and concomitant large increase in splenic blood flow after haemorrhage in intact, awake rats. Catecholamines from the adrenal glands did not contribute detectably to the splenic vasodilation.