Effect of subarachnoid hemorrhage on dilatation of rat basilar
artery in vivo.
Sobey, Christopher G., Donald D. Heistad, and Frank M. Faraci.
Departments of Internal Medicine and Pharmacology, Cardiovascular
Research Center, and Center on Aging, University of Iowa College of
Medicine, Iowa City, Iowa 52242
APStracts 2:0566H, 1995.
Dilator responses of the basilar artery are often impaired in
experimental models of subarachnoid hemorrhage (SAH). Because
depolarization of vascular muscle may occur after SAH, we examined
responses to a stimulus that produces hyperpolarization of vascular
muscle. We tested in vivo the hypothesis that SAH may augment
dilatation in response to activation of potassium channels.
Anesthetized rats were studied 2 days after injection of 0.3 - 0.5 ml
saline or autologous blood into the cisterna magna. Diameter of the
basilar artery in vivo was 224+5 [mu]m (mean+SE) in saline-treated
rats and 201+6 [mu]m in SAH rats (p<0.05). In control rats,
acetylcholine, sodium nitroprusside, aprikalim and calcitonin gene
-related peptide (CGRP; both activators of ATP-sensitive potassium
channels), papaverine, 8-bromo-cyclic GMP, and brain natriuretic
peptide (BNP, an activator of particulate guanylate cyclase) produced
concentration-dependent dilatation. In SAH rats, vasodilatation was
impaired in response to acetylcholine (by 67% and 59% at 10-6 M and
10-5 M, respectively) and sodium nitroprusside (by 47% and 30% at 10
-7 M and 10-6 M, respectively). In contrast, vasodilator responses to
aprikalim (1-3 x 10-7 M) and CGRP (10-10 M - 10-9 M) were augmented
in SAH rats (by 2-4 -fold). Vasodilator responses to 8-bromo-cyclic
GMP, papaverine, and BNP were similar in both groups. Thus,
vasodilator mechanisms are selectively altered by SAH. Responses
mediated by nitric oxide-mediated activation of soluble guanylate
cyclase are selectively and profoundly impaired by SAH, but responses
to cyclic GMP are normal. Vasodilator responses to activation of ATP
-sensitive potassium channels are augmented by SAH, perhaps because
the basilar artery is partially depolarized.
Received 22 May 1995; accepted in final form 1 December 1995.
APS Manuscript Number H477-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 December 95