Phospholipid degradation and edema development in cold-injured rat brain

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.