Affiliation:
1. Cerebrovascular Research Center, Department of Neurology, University of Pennsylvania, Philadelphia, Pennsylvania, U.S.A.
Abstract
The effect of hyperglycemia on cytosolic free calcium ([Ca2+]i) during temporary focal cerebral ischemia was investigated in cats using a fluorometric technique. The middle cerebral artery (MCA) was occluded for a period of 1 h, after which the clip was removed. In seven animals, plasma glucose was raised to 500–700 mg/dl by infusion of a 50% glucose solution starting 30 min after MCA occlusion, while eight animals were kept normoglycemic during and following occlusion. MCA occlusion induced a significant, but identical, elevation of the [Ca2+]i signal ratio (400/506 nm) in both the normoglycemic group (from 1.40 to 1.97 ± 0.34, p < 0.01) and in the hyperglycemic group (from 1.40 to 2.00 ± 0.53, p < 0.01) at the end of the occlusion. Between 10 and 30 min after reopening, the [Ca2+]i signal ratio decreased to control levels in the normoglycemic group (1.40 ± 0.11 and 1.36 ± 0.08 at 10 and 30 min after reopening, respectively), but remained elevated in the hyperglycemic group (1.69 ± 0.18 and 1.65 ± 0.21 at 10 and 30 min after reopening, respectively). There was a statistically significant difference between the two groups ( p < 0.01). These data suggest that hyperglycemia may be harmful to calcium recovery during the early recirculation period following focal cerebral ischemia.
Subject
Cardiology and Cardiovascular Medicine,Clinical Neurology,Neurology
Cited by
49 articles.
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