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Free fatty acids (FFA), diacylglycerols (DG), and water content were measured in the right and left cerebral hemispheres of rats with brain edema cryogenically induced to the right cerebral hemisphere. The effect of dexamethasone pretreatment was also studied. Twenty-four hours after lesion, maximal edema was attained concomitant with an accumulation of FFA (8.5-fold) and DG (2.9-fold). Polyunsaturated fatty acids (PUFA), primarily docosahexaenoic acid, increased greatly in both lipid pools. In the contralateral hemisphere, only DG levels increased, especially those containing stearate and arachidonate, which increased by almost 50%. By 48 h, FFA had decreased 60%, whereas DG had attained sham levels. These changes occurred prior to edema resolution. Dexamethasone decreased the degree of edema and the accumulation of PUFA-containing DG by 30% in both hemispheres. There was a complete inhibition of FFA and arachidonic acid accumulation in the lesioned side. These results suggest that dexamethasone: (1) inhibits phospholipases A2 that, in turn, decrease membrane phospholipid breakdown; and (2) has a limited effect on the enzymatic systems involved in PUFA-DG accumulation. Hence, in experimentally induced vasogenic brain edema, PUFA-containing DG, rather than FFA, may be related closely to the spreading of edema fluid. |
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