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Changes in cardiac filling pressure (central venous pressure) were measured following carotid occlusion and infusions of catecholamines in awake dogs while cardiac output was held constant. After carotid occlusion in dogs with vagi blocked, central venous pressure increased about 0.8 mm Hg (an estimated decrease in vascular capacity of 2.4 ml/kg). Carotid occlusion before vagal block or following vagal block and beta-adrenergic block with propranolol caused no significant changes in central venous pressure. Phenylephrine (0.1-2.0 micrograms/min per kg) caused dose-dependent increases in arterial pressure, but changed central venous pressure (ca. 2.5 mm Hg) only at the highest doses. Epinephrine in doses (0.03-0.51 micrograms/min per kg) that caused little change in arterial pressure increased central venous pressure up to 5.3 mm Hg (an estimated decrease in vascular capacity of 12.0 ml/kg); this response was attenuated about 50% by propranolol. Isoproterenol (0.01-0.40 micrograms/min per kg) decreased arterial pressure and caused changes in central venous pressure similar to those seen with epinephrine. These responses were abolished by propranolol. Vascular compliance, determined from the change in central venous pressure following known changes in vascular blood volume, averaged 3.0 +/- 0.6 ml/mm Hg per kg. In the conscious, resting dog, both alpha- and beta-adrenergic receptors are involved in the reflex control of cardiac filling pressure. The beta-adrenergic responses predominate.

Changes in vascular capacity in awake dogs in response to carotid sinus occlusion and administration of catecholamines.