PATHOPHYSIOLOGICAL PROCESS AFTER TRANSIENT ISCHEMIA OF THE MIDDLE CEREBRAL-ARTERY IN THE RAT

For the understanding of pathophysiology of the cerebral ischemia, we made a transient intraluminal occlusion of the middle cerebral artery in the rat and investigated the appearance of collapsed dark neurons a nd the extravasation of serum proteins using argyrophil III method and immunohistochemistry. In the acute stage (minutes to 3 days), dark ne urons appeared in the lateral half of the ipsilateral striatum and adj acent cortex which formed the ischemic core of this model. Dark neuron s also appeared in the ipsilateral reticular thalamic nucleus, hippoca mpus, and amygdala. The extravasation of serum proteins, albumin, leuc ocyte common antigen, immunoglobulin G, complement factor C3, as well as heat shock protein 70, was observed not only in the ischemic but so metimes also in the contralateral hemisphere. Among these, the express ion of IgG and C3 was most prominent in the ischemic core. In the chro nic stage (1 to 3 months), the ischemic core changed into the porencep haly, and the ventrobasal nucleus of the thalamus got also involved in the necrosis. A strong microgliosis was observed in the substantia ni gra pars reticulata. Data suggest, that among many mechanisms that con tribute to ischemic neuronal death, the activation of immune response, due to the damage of blood-brain barrier and the extravasation of ser um proteins could promote the ischemic cell death in the brain.