Phospholipid Degradation and the Early Release of Polyunsaturated Fatty Acids in the Evolution of Brain Edema

Abstract

Using both in vitro cortical slices and in vivo models, we have studied the roles of phospholipid degradation and the release of polyunsaturated fatty acid in the evolution of brain edema. We have shown that pus, i.e., fragmented polymorphonuclear leukocytes and other inflammatory cells, acts as a potent inducer of cellular swelling in brain slices13. The swelling factors were identified as free fatty acids, especially polyunsaturated fatty acids (PUFA)5,8. Linoleic acid (18:2), linolenic acid (18:3), arachidonic (20:4) and docosahexaenoic acid (22:6) caused a two to three-fold increase in tissue swelling concomitant with the increase of intracellular sodium and decrease of intracellular potassium. The extracellular inulin space was also decreased indicating the presence of cellular (cytotoxic) edema. This model of cellular edema was also associated with changes in cellular metabolism since lactic acid levels were elevated and high energy nucleotides were reduced13,5.