Stroke, Vol 25, 165-170, Copyright © 1994 by American Heart Association
G Yang, PH Chan, J Chen, E Carlson, SF Chen, P Weinstein, CJ Epstein and H Kamii
BACKGROUND AND PURPOSE--We have demonstrated in a previous study that
superoxide radicals play a role in the pathogenesis of cerebral infarction,
using a transgenic mouse model of distal middle cerebral artery occlusion,
permanent ipsilateral cerebral carotid artery occlusion, and 1-hour
contralateral cerebral carotid artery occlusion that produced infarction
only in the cortex. However, the role of superoxide radicals in reperfusion
injury in transgenic mice overexpressing superoxide dismutase (SOD) is
unknown. Using a mouse model of intraluminal blockade of middle cerebral
artery that produced both cortical and striatal infarction, we now further
examined the role of superoxide radicals in ischemic cerebral infarction
after reperfusion in transgenic mice overexpressing human CuZn-SOD
activity. METHODS--Transgenic mice of strain Tg HS/SF-218, carrying human
SOD-1 genes, and nontransgenic littermates were anesthetized with chloral
hydrate (350 mg/kg IP) and xylazine (4 mg/kg IP). Physiological parameters
were maintained at a normal range using a 30% O2/70% N2O gas mixture
inserted via an inhalation mask. Body temperature was maintained at 37 +/-
0.5 degrees C by using a heating pad throughout the studies. The middle
cerebral artery occlusion was achieved with a 5- 0 rounded nylon suture
placed within the internal cerebral artery for 3 hours followed by the
removal of the suture to allow reperfusion for another 3 hours. Cerebral
infarct size in brain slices and infarct volume, neurological deficit,
cortical blood flow, and glutathione levels were measured in both
transgenic and nontransgenic mice. RESULTS- -Compared with the
nontransgenic mice, the infarcted areas were significantly decreased in
coronal slices from transgenic mice. The infarct volume (in cubic
millimeters) was reduced by 26% in transgenic mice after ischemia and
reperfusion. This decrease in the infarct volume in transgenic mice closely
paralleled the reduced neurological deficits. Introduction of the suture to
block blood supply to the middle cerebral artery territory produced a rapid
decrease in the relative surface blood flow in the ipsilateral core and the
peri- ischemic (penumbra) areas. There were no significant differences in
the local cerebral blood flow in the ischemic core or the penumbra areas
between the transgenic and nontransgenic groups. However, the level of
reduced glutathione in the penumbra area was significantly higher in
transgenic mice than in nontransgenic mice, whereas there was no difference
in the reduced glutathione levels in the ischemic core between these two
groups. CONCLUSIONS--Our study demonstrated that superoxide radicals play a
major role in the pathogenesis of cerebral infarction in reperfusion injury
after a focal stroke. The reduction in infarct volume and neurological
deficits is not dependent on the changes in cerebral blood flow but rather
correlate with reduced oxidative stress in the ischemic brain tissue, which
was indicated by the relatively high levels of endogenous reduced
glutathione in transgenic mice.
ARTICLES
Human copper-zinc superoxide dismutase transgenic mice are highly resistant to reperfusion injury after focal cerebral ischemia
Department of Neurology, School of Medicine, University of California, San Francisco 94143-0114.
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