Carotid sinus baroreceptor effects on cat livers in control and hemorrhaged states.
Hepatic blood volume, glucose output, and arterial conductance changes were measured in cats in response to unloading carotid sinus baroreceptors using carotid arterial occlusion or perfusion of carotid arteries in situ. Changes in all three parameters are known to be elicited by direct stimulation of the hepatic sympathetic nerves. The baroreflex did not activate glycogen breakdown, whereas nerve stimulation and hemorrhage did, indicating that not only were hepatic nerves not reflexly activated but glucagon and adrenaline levels in plasma were not significantly elevated. Hemorrhage with carotid pressure held constant produced hyperglycemia within a normal range. Hepatic blood volume responses to hemorrhage and to noradrenaline were normal but carotid baroreflexes caused no blood volume response with the vagus cut or intact and with the adrenals intact. The blood volume response to hemorrhage and to reinfusion of blood were normal when the carotid blood pressure was held steady. Hepatic arterial constriction did occur but was sufficient to exactly offset the rise in blood pressure so that blood flow remained unaltered.
D000311:Adrenal Glands / Q000502:physiology; D000818:Animals; D001786:Blood Glucose / Q000032:analysis; D001794:Blood Pressure; D001810:Blood Volume; D002346:Carotid Sinus / Q000502:physiology*; D002415:Cats; D006470:Hemorrhage / Q000503:physiopathology*; D008099:Liver / Q000294:innervation*; D008102:Liver Circulation; D011311:Pressoreceptors / Q000502:physiology*; D012018:Reflex; D014628:Vagotomy; D014655:Vascular Resistance
D001786:Blood Glucose