Effects of antihistaminics on experimental brain edema

Abstract

Histamine has potent effects on cerebral blood vessels which include increased permeability and dilatation. Since its concentrations are found to be increased in brain tissue in different experimental models of brain injury, histamine may act as a mediator of secondary brain damage. Using the cold-lesion model of vasogenic brain edema the effects of application of antihistaminics were studied in rats. Neither mepyramine, an H1 receptor blocker nor zolantidine, an H2 blocker provided any decrease in brain swelling or water content. Experiments with application of dexamethasone yielded a small non-significant decrease of edema while the amino-steroid U74389F did not reduce swelling. The results indicate that histamine is obviously not involved in mediating cold lesion-induced brain edema. Furthermore, generation of lipid peroxides after activation of phospholipase A2 also appears not to have a significant influence on edema in the present study.