Cerebral edema after temporary and permanent middle cerebral artery occlusion in the rat.
OBJECTIVE
The potential of thrombolytic agents to improve outcome after ischemic stroke could be negated if recanalization of an occluded artery exacerbates cerebral edema. We examined whether infarctions associated with reperfusion have more edema than those without reperfusion and whether the time course for the development of cerebral edema varied with and without reperfusion.


METHODS
Infarct volumes were measured 24 hours after permanent and 1, 2, and 3 hours of temporary right middle cerebral artery (MCA) occlusion in spontaneously hypertensive rats. Hemispheric volume, water, sodium, and potassium were measured 3, 6, 12, 24, 36, and 48 hours after permanent and 3 hours of temporary MCA occlusion and also determined 24 hours after permanent and 2 and 3 hours of temporary MCA occlusion.


RESULTS
Minimal tissue damage occurred after 1 hour of temporary ischemia. Infarct sizes were similar after permanent and 3 hours of temporary MCA occlusion and significantly greater than after 2 hours of temporary ischemia. Hemispheric volume, water, and sodium from the infarcted right hemisphere were significantly greater than those from the left hemisphere beginning 6 hours after MCA occlusion and continuing for 48 hours, with a peak at 24 hours. Right hemispheric water measured 24 hours after 2 hours of temporary ischemia was significantly less than after permanent or 3 hours of temporary ischemia.


CONCLUSIONS
This study demonstrates that cerebral edema after focal stroke is related to infarct size and is independent of reperfusion status. The results suggest that exacerbation of cerebral edema will not occur after thrombolytic treatment or spontaneous recanalization of occluded cerebral vessels.
Slivka
A
A
Department of Neurology, Ohio State University, Columbus 43210, USA.
Murphy
E
E
Horrocks
L
L
D000704:Analysis of Variance; D000818:Animals; D001157:Arterial Occlusive Diseases / Q000503:physiopathology*; D001929:Brain Edema / Q000209:etiology / Q000503:physiopathology*; D002539:Cerebral Arterial Diseases / Q000503:physiopathology*; D002536:Cerebral Arteries / Q000502:physiology; D002544:Cerebral Infarction / Q000503:physiopathology*; D002546:Ischemic Attack, Transient / Q000503:physiopathology*; D008297:Male; D051381:Rats; D011918:Rats, Inbred SHR; D015424:Reperfusion; D013997:Time Factors