Adrenergic mechanisms in the cephalic and cerebral circulations of the subhuman primate.

Effects of circulating adrenergic amines on the cerebral circulation remain contraversial. Common carotid (CCF) and internal carotid (ICF) arterial flows were determined electromagnetically in eight lightly anesthetized baboons to evaluate alterations in the cephalic and cerebral vascular beds, respectively. Epinephrine (E), norepinephrine (NE), phenylephrine (PE), and isoproterenol (I) were injected randomly in doses of 10-3, 10-2, 10-1, and 1 mug (base) per kilogram into each carotid artery. Measurements were repeated in four animals after alpha-adrenergic blockade with phenoxybenzamine and in another four animals after beta-adrenergic blockade with propranolol. Baseline CCF was 75 plus or minus 10 (S.E.M.) ml. per minute and ICF was 58 plus or minus 8 ml. per minute. Significant (p smaller than 0.05) CCF changes without arterial pressure alterations occurred with 10-1 mug per kilogram doses. Alpha blockade significantly (p smaller than 0.05) attenuated the effects of E, NE, and PE on CCF while beta blockade significantly (p smaller than 0.05) attenuated the effect of I on CCF. ICF did not change significantly (p greater than 0.05) after injection of any of the vasoactive amines, unless associated with pressure changes at the highest dose. Our data suggest the presence of alpha- and beta-adrenergic receptor sites within the cephalic circulation resulting in significant flow responses to intra-arterial adrenergic amines. The absence of responses in the cerebral circulation suggests that circulating catecholamines do not significantly influence or regulate the cerebral vasculature. In addition the data suggest that use of adrenergic agonists to alter the hemodynamics of the cerebral circulation is limited.