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Stroke, Vol 19, 883-887, Copyright © 1988 by American Heart Association

ARTICLES

Metabolic alterations in rabbit cerebral arteries caused by subarachnoid hemorrhage

T Tsukahara, NF Kassell, K Hongo, RM Lehman and JC Torner
Department of Neurological Surgery, University of Virginia School of Medicine, Charlottesville 22908.

The effect of subarachnoid hemorrhage on metabolic rates in rabbit cerebral arteries was investigated by measuring adenosine triphosphate (ATP) content and L-lactate release. The mean +/- SEM ATP content was 0.38 +/- 0.02 mumol/g wet wt in control rabbit basilar arteries (n = 6). The ATP content decreased significantly to 0.17 +/- 0.02 mumol/g wet wt 2 days after experimental subarachnoid hemorrhage (n = 6), although only a slight decrease was detected in the basilar arteries 2 days after cisternal injection of the same amount of artificial cerebrospinal fluid. Hypoxia significantly decreased ATP content in the control basilar arteries to 0.26 +/- 0.04 mumol/g wet wt (n = 6). The same degree of hypoxia did not decrease ATP content in the basilar arteries after subarachnoid hemorrhage. Release of L-lactate was significantly higher from the arteries after subarachnoid hemorrhage than from the control arteries under both aerobic and hypoxic conditions. Our results indicate that subarachnoid hemorrhage induced an alteration of metabolic rates in rabbit cerebral arteries. The oxygen-requiring pathways to synthesize ATP may be important in control cerebral arteries; however, after experimental subarachnoid hemorrhage, the main pathway in the cerebral arteries may shift from oxygen- requiring pathways to an anaerobic glycolytic pathway.

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