title: The contribution of the beta-adrenergic system to the cardiovascular response to hypovolemia.
abstract: Unanesthetized, chronically instrumented, nonpregnant sheep were studied in periods of progressive blood withdrawal, hypovolemic shock, blood reinfusion, and recovery. Hemodynamic responses were recorded during experiments with an intact beta-adrenergic system (saline solution), beta-adrenergic blockage (propranolol), and beta-adrenergic stimulation (isoxsuprine). With an intact beta-adrenergic system, stepwise bleeding produced a progressive decrease in arterial pressure, stroke volume, and cardiac output and an increase in systemic vascular resistance; heart rate increased initially but fell when hypovolemia became severe. All circulatory parameters returned toward control valves during blood reinfusion and recovery. In animals deprived of beta-adrenergic control, the hemodynamic response to progressive hypovolemia and blood reinfusion was not greatly different from that of control animals, despite abolition of tachycardia. During beta-adrenergic stimulation, arterial pressure and cardiac output fell more rapidly than in control and tachycardia was relatively small; cardiac output and stroke volume rebounded strikingly during reinfusion and recovery. These results support findings of others that the role of the beta-adrenergic system is minor during hypovolemia. When pharmacologically activated, it might play a significant role in the posthypovolemia compensatory mechanisms.
mesh_terms: D000818:Animals; D001803:Blood Transfusion; D001810:Blood Volume; D005260:Female; D006339:Heart Rate / Q000187:drug effects; D006439:Hemodynamics / Q000187:drug effects; D007556:Isoxsuprine / Q000494:pharmacology; D011433:Propranolol / Q000494:pharmacology; D011943:Receptors, Adrenergic, beta / Q000502:physiology*; D012756:Sheep; D012769:Shock / Q000503:physiopathology
chemical_list: D011943:Receptors, Adrenergic, beta; D011433:Propranolol; D007556:Isoxsuprine