Nitric oxide synthase inhibition attenuates hypoglycemic cerebral hyperemia in piglets.
Publication/Presentation Date
3-1-1994
Abstract
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.
Volume
266
Issue
3 Pt 2
First Page
1062
Last Page
1068
ISSN
0002-9513
Published In/Presented At
Ichord, R. N., Helfaer, M. A., Kirsch, J. R., Wilson, D., & Traystman, R. J. (1994). Nitric oxide synthase inhibition attenuates hypoglycemic cerebral hyperemia in piglets. The American journal of physiology, 266(3 Pt 2), H1062–H1068. https://doi.org/10.1152/ajpheart.1994.266.3.H1062
Disciplines
Medicine and Health Sciences | Pediatrics
PubMedID
7512794
Department(s)
Department of Pediatrics
Document Type
Article