Nitro-l-arginine-sensitive regional cerebral blood flow
augmentation during hypercapnia in mice with type iii nitric oxide
synthase gene deletion.
Ma, Jianya, Wei Meng, Cenk Ayata, Paul L. Huang, Mark C. Fishman, and
Michael A. Moskowitz.
Stroke and Neurovascular Regulation Laboratory; Dept. of
Neurosurgery and Neurology; Cardiovascular Research Center*, Dept. of
Medicine; Massachusetts General Hospital, Harvard Medical School,
Charlestown, MA, 02129
APStracts 3:0282H, 1996.
The effect of nitro-L-arginine (L-NA) on regional cerebral blood flow
(rCBF) response to hypercapnia (5%CO2 inhalation) was studied in
urethane-anesthetized wild type (SV-129) and type III NOS deficient
mice using laser Doppler flowmetry and the closed cranial window
technique. Resting rCBF during normocapnia decreased by approximately
25% following L-NA superfusion in wild-type mice only (n=18),
suggesting a role for type III NOS on baseline blood flow.
Hypercapnia augmented rCBF approximately 50% in both wild-type and
type III NOS mutant mice. L-NA superfusion (1mM) inhibited this
increase by approximately 60% in both strains. Hence, synthesis of NO
by the constitutively expressed type I NOS contributes to blood flow
augmentation during hypercapnia.
Received 20 May 1996; accepted in final form 28 June 1996.
APS Manuscript Number H463-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996