Nitric oxide synthase inhibition attenuates hypoglycemic cerebral hyperemia in piglets

R. N. Ichord, M. A. Helfaer, J. R. Kirsch, D. Wilson, R. J. Traystman

Research output: Contribution to journalArticle

32 Scopus 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 iv) with and without an NO synthase inhibitor, N(ω)-nitro-L-arginine methyl ester (L-NAME, 40 mg/kg iv). Electroencephalogram (EEG), cerebral O2 consumption (CMR(O2)), 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 CMR(O2). L-NAME prevented the increase in CMR(O2) 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.

Original languageEnglish (US)
Pages (from-to)H1062-H1068
JournalAmerican Journal of Physiology - Heart and Circulatory Physiology
Volume266
Issue number3 35-3
DOIs
StatePublished - 1994

Keywords

  • N(ω)-nitro-L-arginine methyl ester
  • cerebral blood flow
  • electroencephalogram
  • hypoglycemia
  • infant

ASJC Scopus subject areas

  • Physiology
  • Cardiology and Cardiovascular Medicine
  • Physiology (medical)

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