Reperfusion enhances nitrotyrosine formation in rat focal cerebral ischemia.

The widespread benefit of thrombolysis has been emphasized, but relatively little is known about reperfusion injury. The purpose of this study is to evaluate the difference in nitrotyrosine formation and infarct volume between permanent and transient focal ischemia in rats. Permanent (n = 14) or transient (n = 12) focal ischemia was induced by permanent or 2-hour occlusion of the middle cerebral artery, respectively, with the permanent ligation of the bilateral common carotid arteries in Sprague-Dawley rats. In both models all animals were killed 24 hours after the start of occlusion. The ratio of nitrotyrosine in the peri-infarct and core-of-infarct regions in transient focal ischemia was significantly higher than in permanent focal ischemia (P < .01). Infarct volume in the cortex, but not caudoputamen or whole brain, was significantly larger in transient ischemia than in permanent ischemia (P < .05), with a significant expansion of brain swelling. These results may reflect the higher production of superoxide and nitric oxide owing to reperfusion, and suggest the need to administer neuroprotective drugs such as anti-oxidants as well as thrombolytic agents in the treatment of acute ischemic cerebral damage.