Neuronally derived nitric oxide promotes cerebral cortical
hyperemia during cortical spreading depression in anesthetized
rabbits.
Colonna, David M., Wei Meng, Dwight D. Deal, Mamatha Gowda, and David
W. Busija.
Department of Anesthesia; Department of Physiology and
Pharmacology, and Neuroscience Center, Bowman Gray School of
Medicine, Wake Forest University, Winston-Salem, NC 27157-1009;
Stroke and Neurovascular Regulation Lab, Massachusetts General,
Hospital, Harvard Medical School, Charlestown, MA 02129
APStracts 3:0444H, 1996.
Temporary elevations of cortical cerebral blood flow (CBF) accompany
cortical spreading depression (CSD) in anesthetized animals. We
tested the hypothesis that nitric oxide (NO x ) is an important
promotor of CSD induced cortical hyperemia in urethane anesthetized
rabbits. CBF was measured at four time points by administration of
15[mu]m microspheres, using the reference withdrawal technique.
Intravenous administration of the nonspecific NO x S inhibitor, N_
-nitro-L-arginine (L-NA) increased mean arterial blood pressure (MABP)
and resting cerebrovascular resistance (CVR), and attenuated CSD
induced hyperemia. Cortical CBF before intraperitoneal 7
-nitroindazole (7-NI), a neuronal NO x synthase (nNO x S) inhibitor,
was 42 +/- 8 and 124 +/- 19 ml x 100g-1 x min at baseline and during
CSD, respectively (p < 0.05, RM-ANOVA). After 7-NI
administration, MABP, CBF and CVR were unchanged from baseline
values; cortical CBF was 38 +/- 4 and 90 +/- 8 ml x 100g-1 x min post
7-NI at rest and during a second CSD, respectively. Similar to L-NA,
7-NI decreased the cortical hyperemic response during CSD (p <
.05, RM-ANOVA). We conclude that nNO x S promotes the temporary
cortical hyperemia observed during CSD.
Received 20 May 1996; accepted in final form 11 October 1996.
APS Manuscript Number H454-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 5 November 1996