(Stroke. 1995;26:627-635.)
© 1995 American Heart Association, Inc.
Articles |
Neurological Deficit and Extent of Neuronal Necrosis Attributable to Middle Cerebral Artery Occlusion in Rats
Statistical Validation
From the Department of Pathology (Neuropathology), Henry Ford Hospital, Detroit, Mich (J.H.G., S.W., K.-F.L., X.H.), and Case Western Reserve University, Cleveland, Ohio (J.H.G.).
Correspondence to Julio H. Garcia, MD, Department of Pathology (Neuropathology), Henry Ford Hospital/K-6, 2799 W Grand Blvd, Detroit, MI 48202-2689.
Background and Purpose Occluding a large intracranial artery in rats produces a brain lesion that grows in terms of an increase in both surface area and number of necrotic neurons. The present study investigated whether reperfusing the ischemic territory 30 to 60 minutes after the arterial occlusion would have a beneficial effect on either the clinical or the histological outcome of the lesion.
Methods One hundred four adult rats (including appropriate controls) were used; 97 had a middle cerebral artery occluded by inserting a nylon monofilament via the right external carotid artery. The arterial occlusion was transient in two groups and permanent in another; survival times were comparable for all groups. Control animals were subjected to a sham operation during which the artery was occluded for less than 1 minute. The outcome was evaluated by measuring the extent of the neurological deficit and the severity of the histological injury.
Results Mean neurological score and mean number of necrotic neurons in the cortex were more favorable after transient (30- to 60-minute) compared with permanent arterial occlusion (P<.005). Moreover, the correlation between mean neurological score and mean number of necrotic neurons was highly significant: r=.951; P<.001.
Conclusions The histological effects of an intracranial arterial
occlusion in the adult rat can be predicted on day 1 by the
neurological score described in this report. Significant improvement
can be obtained in these animals by reestablishing arterial flow 60
minutes or sooner after the ictus. The pattern of cortical pannecrosis
observed after permanent occlusion (
72 hours) was transformed into
incomplete ischemic injury in most instances of transient occlusion.
Key Words: cerebral infarction • cerebral ischemia • neuronal damage • reperfusion • rats
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