Jh. Garcia et al., NEUROLOGICAL DEFICIT AND EXTENT OF NEURONAL NECROSIS ATTRIBUTABLE TO MIDDLE CEREBRAL-ARTERY OCCLUSION IN RATS - STATISTICAL VALIDATION, Stroke, 26(4), 1995, pp. 627-634
Background and Purpose Occluding a large intracranial artery in rats p
roduces a brain lesion that grows in terms of an increase in both surf
ace area and number of necrotic neurons. The present study investigate
d whether reperfusing the ischemic territory 30 to 60 minutes after th
e arterial occlusion would have a beneficial effect on either the clin
ical or the histological outcome of the lesion. Methods One hundred fo
ur adult rats (including appropriate controls) were used; 97 had a mid
dle cerebral artery occluded by inserting a nylon monofilament via the
right external carotid artery. The arterial occlusion was transient i
n two groups and permanent in another; survival times were comparable
for all groups. Control animals were subjected to a sham operation dur
ing 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 sco
re and mean number of necrotic neurons in the cortex were more favorab
le after transient (30- to 60-minute) compared with permanent arterial
occlusion (P<.005). Moreover, the correlation between mean neurologic
al 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 c
an be obtained in these animals by reestablishing arterial flow 60 min
utes or sooner after the ictus. The pattern of cortical pannecrosis ob
served after permanent occlusion (greater than or equal to 72 hours) w
as transformed into incomplete ischemic injury in most instances of tr
ansient occlusion.