Nitric oxide synthase inhibition by L-NAME prevents brain acidosis during focal cerebral ischemia in rabbits

Détails

ID Serval
serval:BIB_CC3F638D8E01
Type
Article: article d'un périodique ou d'un magazine.
Collection
Publications
Titre
Nitric oxide synthase inhibition by L-NAME prevents brain acidosis during focal cerebral ischemia in rabbits
Périodique
Journal of Cerebral Blood Flow and Metabolism
Auteur(s)
Regli  L., Held  M. C., Anderson  R. E., Meyer  F. B.
ISSN
0271-678X (Print)
Statut éditorial
Publié
Date de publication
09/1996
Volume
16
Numéro
5
Pages
988-95
Notes
Journal Article
Research Support, Non-U.S. Gov't
Research Support, U.S. Gov't, P.H.S. --- Old month value: Sep
Résumé
This experiment examined the effects of nitric oxide (NO) synthase inhibition on brain intracellular pH, regional cortical blood flow, and NADH fluorescence before and during 3 h of focal cerebral ischemia using in vivo fluorescence imaging. Thirty fasted rabbits under 1% halothane were divided into four treatment groups receiving N omega-nitro-L-arginine methyl ester (L-NAME) intravenously at 20 min prior to ischemia (0.1, 1, and 10 mg/kg and 1 mg/kg + 5 mg/kg L-arginine) and two control groups (nonischemic and ischemic). In ischemic controls, brain pH(i), declined to 6.73 +/- 0.03 at 30 min and remained acidotic through the remainder of the ischemic period. In the 0.1 mg/kg group, brain pH(i) fell after 30 min of ischemia to 6.76 +/- 0.05 (p < 0.05), but then improved progressively despite occlusion. In the 1 mg/kg group, brain pH(i), remained normal despite middle cerebral artery (MCA) occlusion. In the 10 mg/kg group and in the combined L-NAME + L-arginine group, pH(i) fell after 30 min of ischemia to 6.81 +/- 0.03 (p < 0.05) and remained acidotic. During occlusion, regional cortical blood flow dropped in a dose-dependent manner. After 3 h of ischemia, regional cortical blood flow was 33.9 +/- 10.9 and 25.1 +/- 8.9 ml/100 g/min at doses of 0.1 and 10.0 mg/kg, respectively, L-NAME treatment did not significantly alter the increased NADH fluorescence that accompanied occlusion. This study shows that L-NAME can prevent intracellular brain acidosis during focal cerebral ischemia independent from regional cortical blood flow changes. This experiment suggests that NO is involved in pH(i) regulation during focal cerebral ischemia.
Mots-clé
Acidosis/etiology/*prevention & control Animals Arginine/*analogs & derivatives/pharmacology/therapeutic use Brain Diseases/etiology/*prevention & control Cerebral Cortex/blood supply Enzyme Inhibitors/*therapeutic use Fluorescence Hydrogen-Ion Concentration Ischemic Attack, Transient/*complications NAD/metabolism NG-Nitroarginine Methyl Ester Nitric Oxide Synthase/*antagonists & inhibitors Rabbits Umbelliferones
Pubmed
Web of science
Création de la notice
25/01/2008 14:10
Dernière modification de la notice
03/03/2018 21:28
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