Stroke, Vol 22, 1312-1316, Copyright © 1991 by American Heart Association
DN Dao, M Ahdab-Barmada and NF Schor
BACKGROUND: Glutamate has been implicated in the pathophysiology of acute
hypoxic-ischemic encephalopathy. Glutamine synthetase is an enzyme found in
astrocytes that converts glutamate to its nontoxic analogue, glutamine. The
present study tests the hypothesis that brain glutamine synthetase activity
increases in response to acute hypoxic- ischemic insults and not in
response to chronic hypoxia-ischemia or non- hypoxic-ischemic neurological
disease. SUMMARY OF REPORT: Frozen sections of cerebellum from children who
died with acute or chronic hypoxic-ischemic insults or chronic
non-hypoxic-ischemic neurological disease were spectrophotometrically
assayed for glutamine synthetase activity by an observer who was blinded to
the clinical group assignment of each specimen. Enzyme activity was
elevated in specimens from children with acute hypoxic-ischemic insults
(mean 6.5; range 5.4- 7.2 units/g wet tissue wt) as compared with those
from patients with chronic hypoxia-ischemia (mean 2.8; range 0.7-10.2
units/g wet tissue wt) or with non-hypoxic-ischemic neurological disease
(mean 2.6; range 1.3-3.9 units/g wet tissue wt). This difference was not
due to differences in the degree of histological astrocytosis or edema
among the specimens. Statistical analysis by the Kruskal-Wallis one-way
analysis of variance by ranks test indicates that the three data groups do
not come from one population (p less than 0.05). CONCLUSIONS: These results
support the notion that glutamine synthetase activity increases in response
to acute hypoxic-ischemic nervous system injury in children and that other
compensatory mechanisms prevail in the case of chronic hypoxic-ischemic
insults.
ARTICLES
Cerebellar glutamine synthetase in children after hypoxia or ischemia
Department of Pediatrics, University of Pittsburgh, PA.
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