Nitro-L-arginine attenuates hypercapnic cerebrovasodilation without affecting cerebral metabolism

Nitro-L-arginine attenuates hypercapnic cerebrovasodilation without affecting cerebral metabolism Minnesota Iadecola, Costanti, Xiaohong Xu. Nitro-Larginine attenuates without affecting cerebral metabolism. Am. J. Physiol. 266 (Regulatory Integrative Comp. Physiol. 35): R518-R525, 1994.-We have previously demonstrated that topical cortical application of nitro-L-arginine ‘(L-NA), a potent inhibitor of nitric oxide () synthesis, attenuates resting cerebral blood flow (CBF) the elicited by hypercapnia. In this study, we sought to determine whether these cerebrovascular effects of L-NA are secondary to a depression in cerebral metabolism. Rats were anesthetized (chloralose, 80 mg/kg) artificially ventilated. Arterial pressure blood gases were monitored. The frontal cortex was exposed superfused with rmal (pH 7.3-7.4; 37°C) or with containing L- or D-NA. CBF or cerebral glucose utilization (CGU) was measured autoradiographically using the [ 14C]iodoantipyrine or 2-[14C]deoxy-D-glucose method, respectively. Application of rmal did t affect CBF at the site of superfusion (n = 5; P > 0.05, paired t test). Application of L-NA (1 mM; n = 5), but t D-NA (1 mM; n = 6), attenuated resting CBF by 33 t 5% (P < 0.05; analysis of variance). During hypercapnia (partial pressure of CO2 = 55-60 mmHg), L-NA attenuated the CBF increase by 78 t 6% (n = 5/group; P < 0.05 from ), whereas D-NA had http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Regulatory, Integrative and Comparative Physiology The American Physiological Society

Nitro-L-arginine attenuates hypercapnic cerebrovasodilation without affecting cerebral metabolism

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Publisher
The American Physiological Society
Copyright
Copyright © 1994 the American Physiological Society
ISSN
0363-6119
eISSN
1522-1490
Publisher site
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Abstract

Minnesota Iadecola, Costanti, Xiaohong Xu. Nitro-Larginine attenuates without affecting cerebral metabolism. Am. J. Physiol. 266 (Regulatory Integrative Comp. Physiol. 35): R518-R525, 1994.-We have previously demonstrated that topical cortical application of nitro-L-arginine ‘(L-NA), a potent inhibitor of nitric oxide () synthesis, attenuates resting cerebral blood flow (CBF) the elicited by hypercapnia. In this study, we sought to determine whether these cerebrovascular effects of L-NA are secondary to a depression in cerebral metabolism. Rats were anesthetized (chloralose, 80 mg/kg) artificially ventilated. Arterial pressure blood gases were monitored. The frontal cortex was exposed superfused with rmal (pH 7.3-7.4; 37°C) or with containing L- or D-NA. CBF or cerebral glucose utilization (CGU) was measured autoradiographically using the [ 14C]iodoantipyrine or 2-[14C]deoxy-D-glucose method, respectively. Application of rmal did t affect CBF at the site of superfusion (n = 5; P > 0.05, paired t test). Application of L-NA (1 mM; n = 5), but t D-NA (1 mM; n = 6), attenuated resting CBF by 33 t 5% (P < 0.05; analysis of variance). During hypercapnia (partial pressure of CO2 = 55-60 mmHg), L-NA attenuated the CBF increase by 78 t 6% (n = 5/group; P < 0.05 from ), whereas D-NA had

Journal

AJP - Regulatory, Integrative and Comparative PhysiologyThe American Physiological Society

Published: Feb 1, 1994

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