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(Stroke. 1971;2:219.)
© 1971 American Heart Association, Inc.

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Adrenergic Blockade of Hypocapnic Cerebral Arterial Constriction

RICHARD A. R. FRASER M.D.¹; BENNETT M. STEIN M.D.¹; J. LAWRENCE POOL M.D.¹

¹ Department of Neurological Surgery, Columbia University, Neurological Institute of New York, 710 West 168th Street, New York, New York, 10032

Hypocapnic constriction of the basilar and vertebral arteries was produced and pharmacologically modified (by intrathecal administration) in nine Rhesus monkeys. The arteries were then removed and studied with a catecholamine fluorescent technique. Alterations in P_COCO2 were associated with significant changes in the caliber of large arteries. Mere depletion of the periarterial norepinephrine stores did not prevent hypocapnic vasoconstriction. The latter was reversed, however, by alpha adrenergic blockade (phenoxybenzamine). The alpha adrenergic receptor appears to be a mediating site for hypocapnic constriction of the intracranial vessels. We have proposed that the alpha receptor may be H+ sensitive so that changes in pH alter the responsiveness of the adrenergic receptor to transmitter substances.

Key Words: cerebral blood flow • phenoxybenzamine • alpha receptor • catecholamine fluorescence • autoregulation