Experimental brain edema produced by exposure to air. Part I.Changes in water content, local blood flow, and electricalactivity of the cortex, white matter and thalamus.

The present experiment was designed to examine the effect of vasogenic brain edema produced by exposure to air on the electrical activity of the thalamocortical pathway and local cerebral blood flow (1CBF) measured by the hydrogen clearance method. A large area of unilateral cerebral hemisphere of anaesthetized cats was exposed to air for 12 hours, and vasogenic brain edema was produced in the cortical and subcortical structure.Water content of the primary sensorimotor cortex, white matter, and thalamus, which was measured by the specific gravity method, significantly increased by 1.9,4.1,and 0.7% g water/g tissue, respectively, after 12 hours of exposure to air. After six hours of exposure, the blood flow in the cortex, white matter, and thalamus significantly decreased from control levels of 56.8±12.7, 21.7±5,2, 44,1±13.4ml/100g/min to 46.5±13.2, 16.3±5.0, and 31.3±11.9ml/100g/min, respectively. These decreases were accompanied by diminution in the amplitude of the direct cortical responses (DCRs) and prolongation of N1 latencies of the somatosensory evoked responses (SERs) recorded at the primary sensorimotor cortex. Both electrical activities were progressively suppressed in proportion to the reduction of ICBF after six hours of exposure. These results suggest that thalamocortical ischemia is probably responsible for the neural electrical suppression observed in this experimental edema.There was a significant correlation between the amount of edema and the degree of ischemia in the white matter. Accumulation of the edema fluid may induce ischemia affecting sensory conduction through the white matter as suggested by prolongation of the N1 latency of SER.