Abstract
Focal cerebral ischemia was produced in anesthetized rats by a minimally invasive photothrombic procedure. Rose bengal was injected into a tail vein and the right middle cerebral artery region irradiated for 5 min through the skull with the right common carotid artery temporarily occluded. This resulted in focal cerebral infarction which was restricted to the cortex as shown by autoradiography and histopathology. Edema and the uptake of 45Ca were determined 1, 3 or 24 hours after ischemia in different regions of the brain, ipsilateral and contralateral to the ischemic injury, the tracer uptake at three time points after administration. The values of 45Ca uptake and edema were the highest at the center of the infarction. Simulation of the 45Ca uptake kinetics in the 24 h post-ischemic group, enabled -the determination of the contributions of different physiological pathways to cerebral calcium flux. The results indicated the breakdown of the blood-brain barrier to be primarily responsible for the increased uptake of the tracer by the ischemic cortex. A concomitant, presumably intracellular, sequestration resulted in a ca. 76-fold increase in the tissue pool ofexchangeable calcium. Simulation such as proposed here would be of value in predicting the outcome of tracer accumulation in pathological situations [Neural Res 1998; 20: 169–177]
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