Stab-wounded ethanol-intoxicated and non-intoxicated albino rats subjected to chlorpromazine or dexamethasone treatment were studied with respect to blood-brain barrier (BBB) dysfunction. Fifteen h after inflicting large cerebral stab wounds (diameter 400 microns), the animals were intoxicated with ethanol by ip injections or kept as non-intoxicated controls. One h later, the animals were either subjected to intravenous injections of chlorpromazine or dexamethasone or kept as non-treated controls. After intravenous injection of Evans blue-labelled albumin (EBA) or bovine serum albumin only, the rats were killed by intra-aortal perfusion and the BBB dysfunction was studied by fluorescence microscopy or measured by rocket immunoelectrophoresis. In the non-intoxicated group, fluorescence microscopy revealed a considerable decreased area showing extravasation of EBA around the stab wound in rats treated with chlorpromazine. In ethanol-intoxicated, compared to non-intoxicated rats, the area showing extravasation of EBA was not enhanced as studied by fluorescence microscopy. This extravasation was substantially decreased by chlorpromazine treatment, but not affected by dexamethasone. Immunoelectrophoretic assays of the amount of albumin extravasated around the stab wound confirmed the effect of chlorpromazine on the blood-brain barrier dysfunction to bovine albumin in both ethanol-intoxicated and non-intoxicated rats.