The Pathophysiological Basis of Brain Bulk Enlargement Following Decompression

The purpose of this study was to further determine pathophysiological hasis of postdecompressive brain bulk enlargement（BBE）through the experiment of brain compression. 36 cats were divided into 3 groups according to the duration of global ischemia （flat EEG and no CBF）, i, e. acute BBE with 25 minutes of ischemia, delayed BBE with 15 minutes of ischimia and no BBE with 5 minutes of ischemia 12 cats were included in each group. 6 cats were sacrificed in the end of experiment for histological examination, and other 6 cats were injected with 2% Evans blue （4 mg/Kg） and sacrificed at one hour later （3 cats） and the end of experiment （3 cats） respectively. Histologically, the vascular damage, dilation, bleeding and neuronal necrosis were found prominently in brain stem and hypothalamus in acute BBE. CereBral ischemic edema was observed mainly in gray and white matter of cerebral hemispheres in delayed BBE. Evans blue was deeply stained in brain stem and hypothalamus in acute BBE comparing to cerebral hemispheres in delayed BBE. These results disclosed that vasomotor paralysis caused by damage and edema of brain stem and hypothalamus to increase cerebral blood volume was responsible for the pathophysiological basis of acute BBE. Delayed BBE was postulated due to cerebral ischemic edema to increase cerebral water content.