Phospholipid degradation and edema development in cold-injured rat brain

Abstract

Development of brain edema following various pathological insults occurs after some delay. The mechanism of the delay is poorly understood. Using an in vivo model of cold-injury to study the time course of edema development, the present study indicates that the initiation of phospholipid degradation and rapid release of endogenous polyunsaturated fatty acids occurs within 1 min. Evans blue staining was slightly increased in the lesioned area at 1 min and was more profound at 30 min and at 24 h. The cerebral water content was unchanged at 1 min but was significantly increased at later times. The content of thiobarbituric acid-reactive malondialdehyde (MDA) was normal at 1 min but decreased at 30 min and at 24 h. The lipid-soluble fluorescence of MDA conjugates was also decreased concomitant with the degradation of membrane phospholipids at 24 h. Furthermore, Na +, K +-ATPase activities were consistently decreased in traumatized cortex from 24 h to 48 h after the cold-injury. These data indicate that the degradation of membrane phospholipids, the rapid release of polyunsaturated fatty acids and increased blood-brain barrier permeability are very early events underlying the subsequent development of vasogenic edema induced by cold-injury.