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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:â (), 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 mmâ{ (), 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
AJP - Heart and Circulatory Physiology – The American Physiological Society
Published: Nov 1, 1992
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