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AJP - Heart and Circulatory Physiology, Vol 266, Issue 3 1062-H1068, Copyright © 1994 by American Physiological Society
ARTICLES |
R. N. Ichord, M. A. Helfaer, J. R. Kirsch, D. Wilson and R. J. Traystman
Department of Neurology, Johns Hopkins Medical Institutions, Baltimore, Maryland 21287.
We tested the hypothesis that nitric oxide (NO) mediates hypoglycemia-induced cerebral vasodilation in piglets. Piglets (1-2 wk old) were made hypoglycemic with insulin (200 U/kg i.v.) with and without an NO synthase inhibitor, N omega-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg i.v.). Electroencephalogram (EEG), cerebral O2 consumption (CMRO2), and cerebral blood flow (CBF) were measured before L-NAME and insulin and for 180 min after insulin. Hypoglycemia led to isoelectric EEG earlier after L-NAME (87 +/- 8 min) than without L-NAME pretreatment (132 +/- 13 min). CBF increased in all brain regions during hypoglycemia at the onset of isoelectric EEG and was associated with increased CMRO2.L-NAME prevented the increase in CMRO2 and attenuated vasodilation in forebrain (154 +/- 37 vs. 400 +/- 60%), cerebellum (251 +/- 52 vs. 386 +/- 52%), and cortical gray matter (183 +/- 47 vs. 524 +/- 93%) but had no effect on CBF responses in brain stem, thalamus, caudate, or hippocampus. We conclude that NO or a NO-containing compound mediates cerebral vasodilation induced by profound insulin-hypoglycemia in piglets and that this vasodilation plays an important role in the adaptation of immature brain to hypoglycemia.
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R. J. Traystman, L. E. Moore, M. A. Helfaer, S. Davis, K. Banasiak, M. Williams, and P. D. Hurn Nitro-L-Arginine Analogues : Dose- and Time-Related Nitric Oxide Synthase Inhibition in Brain Stroke, May 1, 1995; 26(5): 864 - 869. [Abstract] [Full Text]
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