Exo-focal neuronal death in the rat brain

We describe delayed neuronal damage in ipsilateral remote areas outside the ischemic area of rat brain after transient focal ischemia. The distribution of the neuronal damage was determined by using the 45Ca autoradiographic technique and the histological method, and we investigated the mechanism involved by measuring local cerebral glucose metabolism. Wistar rats were used throughout the experiments. Under 2% halothane anesthesia with a mixture of 70% N2O and 30% O2, the right middle cerebral artery (MCA) was embolized by insertion from the internal carotid artery of a nylon surgical thread with a cylindrical coating of silicone on the distal portion. Animals were divided into 4 groups based on duration of ischemia. After 15, 30, 60 and 90 min of MCA occlusion, recirculation was achieved by removal of the embolus. Immediately after recirculation and then after 24 hr, 3 days, 1 week and 2 weeks of recirculation, 300 microCi 45CaCl2 in aqueous solution (0.3 ml) was administered intravenously; 6 hr later, animals were decapitated to obtain autoradiograms. Histological examination was carried out according to the same protocol. In the 15-min MCA occlusion group, neither 45Ca accumulation nor histological change was observed. In the 30-min MCA occlusion group, 45Ca accumulation extended from the lateral margin to the lateral segment of the caudate-putamen and the cerebral cortex supplied by the occluded MCA depending on the duration of recirculation.(ABSTRACT TRUNCATED AT 250 WORDS)