Protection by Hypothermia of Hypoxia-Induced Inhibition of Neurogenic Vasodilation in Porcine Cerebral Arteries

Porcine cerebral arterial strips denuded of the endothelium responded to transmural electrical stimulation (5 Hz for 40 s) with a relaxation, which was abolished by tetrodotoxin and N G-nitro-L-arginine, a NO synthase inhibitor. Lowering the temperature of the bathing media from 37°C to 33°C or 25°C...

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Main Authors: Toshiki Tanaka, Kazuhide Ayajiki, Hideyuki Fujioka, Noboru Toda, Tomio Okamura
Format: Article
Language:English
Published: Elsevier 2003-01-01
Series:Journal of Pharmacological Sciences
Online Access:http://www.sciencedirect.com/science/article/pii/S1347861319326702
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spelling doaj-edf670e993db402da21497a528c34fcd2020-11-24T21:49:57ZengElsevierJournal of Pharmacological Sciences1347-86132003-01-019229399Protection by Hypothermia of Hypoxia-Induced Inhibition of Neurogenic Vasodilation in Porcine Cerebral ArteriesToshiki Tanaka0Kazuhide Ayajiki1Hideyuki Fujioka2Noboru Toda3Tomio Okamura4Department of Pharmacology, Shiga University of Medical Science, Seta, Ohtsu 520-2192, JapanDepartment of Pharmacology, Shiga University of Medical Science, Seta, Ohtsu 520-2192, JapanDepartment of Pharmacology, Shiga University of Medical Science, Seta, Ohtsu 520-2192, JapanDepartment of Pharmacology, Shiga University of Medical Science, Seta, Ohtsu 520-2192, JapanDepartment of Pharmacology, Shiga University of Medical Science, Seta, Ohtsu 520-2192, JapanPorcine cerebral arterial strips denuded of the endothelium responded to transmural electrical stimulation (5 Hz for 40 s) with a relaxation, which was abolished by tetrodotoxin and N G-nitro-L-arginine, a NO synthase inhibitor. Lowering the temperature of the bathing media from 37°C to 33°C or 25°C potentiated the response to nerve stimulation, but did not affect relaxations induced by NO applied exogenously. Hypoxia suppressed the stimulation-induced relaxation at 37°C, but hypothermia blunted the inhibitory effect of hypoxia in a temperature-dependent manner. It is concluded that hypothermia augments vasodilatation associated with nitroxidergic (nitrergic) nerve activation possibly by increasing the production of NO from L-arginine and, in addition, prevents impairment of NO production by hypoxia. These mechanisms likely explain how hypothermia protects nerve cells against hypoxia. Inhibitions of cyclic GMP phosphodiesterase and of superoxide production by hypoxia do not seem to participate in the action of hypothermia. Mechanisms underlying its protective action remain to be ascertained.http://www.sciencedirect.com/science/article/pii/S1347861319326702
collection DOAJ
language English
format Article
sources DOAJ
author Toshiki Tanaka
Kazuhide Ayajiki
Hideyuki Fujioka
Noboru Toda
Tomio Okamura
spellingShingle Toshiki Tanaka
Kazuhide Ayajiki
Hideyuki Fujioka
Noboru Toda
Tomio Okamura
Protection by Hypothermia of Hypoxia-Induced Inhibition of Neurogenic Vasodilation in Porcine Cerebral Arteries
Journal of Pharmacological Sciences
author_facet Toshiki Tanaka
Kazuhide Ayajiki
Hideyuki Fujioka
Noboru Toda
Tomio Okamura
author_sort Toshiki Tanaka
title Protection by Hypothermia of Hypoxia-Induced Inhibition of Neurogenic Vasodilation in Porcine Cerebral Arteries
title_short Protection by Hypothermia of Hypoxia-Induced Inhibition of Neurogenic Vasodilation in Porcine Cerebral Arteries
title_full Protection by Hypothermia of Hypoxia-Induced Inhibition of Neurogenic Vasodilation in Porcine Cerebral Arteries
title_fullStr Protection by Hypothermia of Hypoxia-Induced Inhibition of Neurogenic Vasodilation in Porcine Cerebral Arteries
title_full_unstemmed Protection by Hypothermia of Hypoxia-Induced Inhibition of Neurogenic Vasodilation in Porcine Cerebral Arteries
title_sort protection by hypothermia of hypoxia-induced inhibition of neurogenic vasodilation in porcine cerebral arteries
publisher Elsevier
series Journal of Pharmacological Sciences
issn 1347-8613
publishDate 2003-01-01
description Porcine cerebral arterial strips denuded of the endothelium responded to transmural electrical stimulation (5 Hz for 40 s) with a relaxation, which was abolished by tetrodotoxin and N G-nitro-L-arginine, a NO synthase inhibitor. Lowering the temperature of the bathing media from 37°C to 33°C or 25°C potentiated the response to nerve stimulation, but did not affect relaxations induced by NO applied exogenously. Hypoxia suppressed the stimulation-induced relaxation at 37°C, but hypothermia blunted the inhibitory effect of hypoxia in a temperature-dependent manner. It is concluded that hypothermia augments vasodilatation associated with nitroxidergic (nitrergic) nerve activation possibly by increasing the production of NO from L-arginine and, in addition, prevents impairment of NO production by hypoxia. These mechanisms likely explain how hypothermia protects nerve cells against hypoxia. Inhibitions of cyclic GMP phosphodiesterase and of superoxide production by hypoxia do not seem to participate in the action of hypothermia. Mechanisms underlying its protective action remain to be ascertained.
url http://www.sciencedirect.com/science/article/pii/S1347861319326702
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