Increased blood-brain barrier permeability around cerebral stab wounds, aggravated by acute ethanol intoxication.

Control and ethanol-intoxicated rats were injured with a small cerebral stab wound and the extravasation of Evans blue-labelled albumin (EBA) was studied. Control rats displayed an extravasation of EBA in the immediate peri-traumatic area with subsequent uptake of EBA in neurons and glia. Ethanol-intoxicated rats showed a greater leakage of EBA as well as a wider area of leaking blood vessels around the stab wound, both in the peri-traumatic and in the early post-traumatic period. Neuronal uptake of EBA was enhanced and observed in a wider area in intoxicated than control rats. The difference in distribution of EBA among neurons and glia between intoxicated and control rats was partly a consequence of the difference in leakage of EBA in the experimental groups. However, part of the increased neuronal uptake of EBA might be explained by an effect of ethanol on nueronal plasmalemma. The results obtained indicated a more pronounced injury to endothelial and neuronal cells after small cerebral stab wounds in ethanol-intoxicated compared to control rats.