Early detection of cerebral ischemic damage and repair process in the gerbil by use of an immunohistochemical technique.

After occlusion of the right common carotid artery in the gerbil, we monitored the progression of ischemic damage and postischemic damage and the repair process in the brain immunohistochemically by using tubulin, creatine kinase BB-isoenzyme (CK-BB), and neuron-specific enolase as the neuronal markers and astroprotein, glial fibrillary acidic protein, and CK-BB as the astrocytic markers. The earliest ischemic lesion was detected in the hippocampus and the cerebral cortex after ischemia for 5 minutes as loss of the reaction in the neuropil, nerve cell bodies, and dendrites. The reaction disappeared more promptly in the dendrites than in the nerve cell bodies. The reaction for tubulin was the most sensitive for detection of the neuronal ischemic damage. After an ischemic period of 30 minutes and subsequent reestablishment of cerebral circulation, the immunohistochemical lesions affecting the neuronal structure expanded during the first 3 hours and then slowly afterward for up to 12 hours. Reactive astrocytes were already identified 24 hours after reperfusion. The current investigation demonstrated that early ischemic damage can be clearly visualized by use of the immunohistochemical technique soon after the onset of cerebral ischemia but that considerable heterogeneity exists not only in different anatomic regions but also within the neuronal structure. This technique has potential for further investigation of cerebral ischemia or other pathophysiologic conditions when used in combination with other morphologic, physiologic, or biochemical techniques.