Faculty Collaboration Database

Nitric oxide synthase inhibition attenuates hypoglycemic cerebral hyperemia in piglets. Am J Physiol 1994 Mar;266(3 Pt 2):H1062-8

Date

03/01/1994

Pubmed ID

7512794

DOI

10.1152/ajpheart.1994.266.3.H1062

Scopus ID

2-s2.0-0028265027 (requires institutional sign-in at Scopus site)   36 Citations

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.

Author List

Ichord RN, Helfaer MA, Kirsch JR, Wilson D, Traystman RJ

MESH terms used to index this publication - Major topics in bold

Amino Acid Oxidoreductases
Animals
Arginine
Cerebrovascular Circulation
Electroencephalography
Glycerol
Hyperemia
Hypoglycemia
Insulin
NG-Nitroarginine Methyl Ester
Nitric Oxide
Nitric Oxide Synthase
Swine