1982 Volume 4 Issue 1 Pages 1-9
The pathophysiology at the center of foci of cerebral infarction was investigated in terms of cerebral blood flow, EEG and histological study. The experimental model for focal cerebral infarction was the thalamic infarction model in the dog. The rCBF was measured using the hydrogen clearance method, simultaneously with recording of thalamic EEG from the same site. Dogs were subjected to temporary vascular occlusion for 30, 60, of 120 minutes, and both rCBF and EEG were recorded for 24 hours after recirculation.
The rCBF of the thalamus was found to be 33±9 ml/min/100g under mild pentobarbital anesthesia. Due to occlusion there was a fall in rCBF to below about 9±2ml/min/100g in the portion of the thalamus showing diminution of fast wave components with attenuation of voltage in EEG recordings. In the dogs with 30 minute temporary occlusion, one showed a transient increase following recirculation but it returned quickly to the control level and was maintained thereafter. Histologically, no infarction was found. In contrast, in the dogs with 60 and 120 minutes temporary occlusion, all showed rCBF values 2-4 times higher than those of controls. Those values decreased with time, but remained high for 24 hours Recovery of thalamic EEG was not seen and histological examination revealed an infarction confined to the thalamus.
