Cerebrovascular mechanisms in perinatal asphyxia: The role of vasogenic brain edema

Abstract

Previous studies from our laboratory have demonstrated penetration of Evan’s blue dye into the brain in profound fetal asphyxia, suggesting that vasogenic brain edema (BE) might be an immediate contributing factor in asphyxial brain injury. We modified the125l- labeled albumin method of Pappius and McCann to quantitate vasogenic BE after acute fetal asphyxia. With51Cr-labeled red cells to measure intravascular volume, and usI-labeled albumin to measure total tissue plasma, the equivalent extra vascular plasma volume, Le., vasogenic BE, was calculated. Twenty chronically prepared animals were studied, six nonasphyxiated controls and 14 asphyxiated (of which six term animals were normotensive and five term and three premature animals were hypertensive during asphyxia). No difference in extra vascular plasma volume was found between asphyxiated and control animals in any of four brain regions. We conclude that, although blood brain barrier function might be impaired, vasogenic BE is not quantitatively significant immediately after severe fetal asphyxia. Speculation: An episode of acute, profound asphyxia in the fetal lamb is not accompanied by the formation of measurable amounts of vasogenic brain edema. Therefore, brain swelling is probably not an important factor in the genesis of acute hypoxic neurologic injury. © 1981 International Pediatric Research Foundation, Inc.