Stroke, Vol 20, 119-122, Copyright © 1989 by American Heart Association
G Sutherland, BY Ong, D Louw and AA Sima
We examined the effect of lidocaine on ischemic neuronal injury in the rat
forebrain ischemia model. Cerebral ischemia was achieved with bilateral
carotid artery occlusion and controlled hypotension to a mean of 50 torr
for 10 minutes. Perfusion-fixation was performed 7 days after ischemia,
subsequent to which the brains were sectioned coronally and stained with
hematoxylin and eosin. Ischemic neuronal injury was quantitatively
expressed (after direct counting) as a percentage of total neurons, that
is, ischemic neurons divided by (ischemic neurons + normal neurons).
Predictably, the selectively vulnerable hippocampal areas exhibited the
most marked neuronal injury. In the CA1/CA2 sectors, lidocaine-treated rats
demonstrated less injury (34 +/- 14%) than untreated (64 +/- 9%) or
saline-treated (70 +/- 10%) rats. However, these superficially pronounced
numerical differences were not of statistical significance (p greater than
0.05). In the CA3 sector, neuronal injury in lidocaine-treated rats (31 +/-
14%) was significantly different at p less than 0.05 from the untreated (80
+/- 5%) but not the saline-treated (59 +/- 13%) group. We conclude that
lidocaine may have an only marginal beneficial effect on forebrain ischemia
in rats.
ARTICLES
Effect of lidocaine on forebrain ischemia in rats
Department of Pharmacology, University of Manitoba, Winnipeg, Canada.
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