HEMORRHAGE-INDUCED SPLENIC VASODILATION IN THE RAT IS MEDIATED BY SYMPATHETIC VASOMOTOR NERVES

A marked decrease in splenic vascular resistance, with an increase in blood flow to the spleen, occurs already 5 min after an acute and seve re hypotensive bleeding in awake rats. This response is virtually abol ished in rats pretreated with a beta-adrenergic blocking agent. We hav e now studied the contribution of the sympathetic vasomotor innervatio n and of adrenal gland-derived catecholamines to the splenic vasodilat ion. Splenic blood Bow was determined with the microsphere method in h eavily bled (1.5% of body weight) awake rats. The sympathetic neurones in one group of rats had been chemically destroyed with 6-hydroxydopa mine. In another group of rats we had removed the adrenal glands. In t he control and in sympathectomized rats, splenic vascular resistance f ell to 35 and 64%, respectively, of baseline 5 min after bleeding. Spl enic blood flow about doubled during this period in the control rats, and then declined gradually to baseline over the next 24 h. In the sym pathectomized rats, splenic blood flow decreased gradually over the fi rst 12 h to reach 66% of baseline. The removal of the adrenal glands d id not appreciably influence the splenic vascular response to bleeding . We conclude that an increased activity in the splenic sympathetic va somotor neurones is a prerequisite for the observed vasodilation and c oncomitant large increase in splenic blood flow after haemorrhage in i ntact, awake rats. Catecholamines from the adrenal glands did not cont ribute detectably to the splenic vasodilation.