Stroke, Vol 20, 1059-1064, Copyright © 1989 by American Heart Association
T Dalkara, IJ Namer, R Onur and T Zileli
Forty rats under urethane anesthesia were subjected to cerebral ischemia by
ligation of the right carotid, the right plus the left carotid, or the
right carotid plus two vertebral arteries. Ischemia caused three types of
changes in the field potential of the right hippocampal CA1 region evoked
by fimbrial stimulation: 1) completely reversible deterioration (57% and
16% of the rats with unilateral and bilateral carotid artery ligation,
respectively), 2) moderate deterioration (37% and 24% of the rats with
unilateral and bilateral carotid artery ligation) and 3) irreversible loss
of the evoked activity (6% and 60% of the rats with unilateral and
bilateral carotid artery ligation and all the rats subjected to
three-vessel occlusion). Naloxone improved the moderate deterioration in 10
of 11 rats (1-3 mg/kg i.v.) and in 15 of 16 (50-150 nA) iontophoretic
applications, but naloxone did not restore the lost evoked activity.
Intravenous morphine (10 mg/kg) aggravated the ischemic changes, and this
effect was reversed by naloxone, while iontophoretic administration of
morphine caused only excitation. These findings suggest that naloxone has a
favorable effect on cerebral ischemia not severe enough to cause
transmission failure. The reversal of ischemic changes by iontophoretic
naloxone indicates that its site of action is at the neuronal or
microcirculatory level.
ARTICLES
Intravenously and iontophoretically administered naloxone reverses ischemic changes in rat hippocampus
Department of Neurology, Hacettepe University Hospitals, Ankara, Turkey.
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