The effect of acute ethanol intoxication and chronic ethanol consumption on vascular permeability around cerebral stab wounds in mice

Summary

It has been suggested that prolongation of a breach in the blood-brain barrier to protein might promote the regeneration of injured axons in the brain and spinal cord. Other workers have found that ethanol given up to 24h after injury will exacerbate exudation of protein from damaged blood vessels in the brains of rats. This raised the possibility that ethanol might be used to maintain cerebral blood vessels in a state of permeability to protein after injury and thus to encourage regeneration of severed central axons.

Stab wounds were made in the brains of mice, and the animals were treated with ethanol for up to 4 weeks. Exudation of protein into the neuropil was detected by use of fluorescently labelled albumin. Single intoxicating doses of ethanol did not increase leakage of the tracer from blood vessels adjacent to lesions that were 3h old. This contrasts with its effect in rats and may be due to a difference in the sensitivity to ethanol of the two species. Ethanol, in the drinking water, increased the extent of exudation of protein around lesions in animals treated for 1 week but had no effect in animals treated for 2, 3 or 4 weeks. Ethanol did not significantly lengthen the period after injury during which the cerebral blood vessels were permeable to protein, so treatment with ethanol would not be expected to support regeneration of damaged axons in the central nervous system (CNS).