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L-arginine decreases infarct size caused by middle cerebral arterial occlusion in SHR

L-arginine decreases infarct size caused by middle cerebral arterial occlusion in SHR Morikawa, Eiharu, Zhihong Huang, and Michael A. Moskowitz. caused by middle cerebral arterial occlusion in SHR. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1632-H1635, 19X-, but not D-arginine, serves as a precursor for the synthesis of nitric oxide (NO), a potent dilator of cerebral blood vessels. We examined the effects of administering (300 mg/kg ip) on the volume of ion in two models of cerebral ischemia in spontaneously hypertensive rats (SHR). was administered before (16 and 3 h) and after (5 min and 2 h) vessel occlusion, and animals were killed 24 h later. treatment decreased in rats subjected to distal middle cerebral arterial (MCA) plus ipsilateral common carotid arterial (CCA) occlusion by 31% [147 t 12 (saline) vs. 101 f: 9 mm:’ (), P < 0.051. D-Arginine, administered according to the same dosage and protocol, was without effect. In the group subjected to proximal MCA occlusion, decreased ion in the striatum by 28% [47 * 5 (saline) vs. 34 & 3 mm’{ (), P < 0.051 and neocortex by 11% [ 193 t 7 (saline) vs. 171 & 8 rnrn:j (), P < 0.051. Changes in blood pressure or other measured physiological parameters did not account http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png AJP - Heart and Circulatory Physiology The American Physiological Society

L-arginine decreases infarct size caused by middle cerebral arterial occlusion in SHR

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Publisher
The American Physiological Society
Copyright
Copyright © 1992 the American Physiological Society
ISSN
0363-6135
eISSN
1522-1539
Publisher site
See Article on Publisher Site

Abstract

Morikawa, Eiharu, Zhihong Huang, and Michael A. Moskowitz. caused by middle cerebral arterial occlusion in SHR. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H1632-H1635, 19X-, but not D-arginine, serves as a precursor for the synthesis of nitric oxide (NO), a potent dilator of cerebral blood vessels. We examined the effects of administering (300 mg/kg ip) on the volume of ion in two models of cerebral ischemia in spontaneously hypertensive rats (SHR). was administered before (16 and 3 h) and after (5 min and 2 h) vessel occlusion, and animals were killed 24 h later. treatment decreased in rats subjected to distal middle cerebral arterial (MCA) plus ipsilateral common carotid arterial (CCA) occlusion by 31% [147 t 12 (saline) vs. 101 f: 9 mm:’ (), P < 0.051. D-Arginine, administered according to the same dosage and protocol, was without effect. In the group subjected to proximal MCA occlusion, decreased ion in the striatum by 28% [47 * 5 (saline) vs. 34 & 3 mm’{ (), P < 0.051 and neocortex by 11% [ 193 t 7 (saline) vs. 171 & 8 rnrn:j (), P < 0.051. Changes in blood pressure or other measured physiological parameters did not account

Journal

AJP - Heart and Circulatory PhysiologyThe American Physiological Society

Published: Nov 1, 1992

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