Vitamin e ameliorates adverse effects of endothelial injury in
brain arterioles.
Rosenblum, William I., Guy H. Nelson, Robert A. Bei, Richard B.
Brandt, Winnie Chan.
Department of Pathology (Neuropathology), Department of
Biochemistry and Molecular Biophysics, Department of Preventive
Medicine, Department of Pediatrics (Pediatric Metabolism, Endocrine
and Genetics)
APStracts 3:0013H, 1996.
Endothelium dependent dilation, produced by applying acetylcholine
(ACh) to pial arterioles, was unaffected after 6 months of a diet
with zero vitamin E or 8 months of an E enriched diet. Nor did the
enriched diet affect constriction produced by topically applied
LNMMA, an inhibitor of the synthesis of "Endothelium Derived
Relaxing Factor" (EDRF). EDRF mediates the response to ACh and is
a basally released dilator and antiplatelet paracrine substance.
Endothelial injury produced by a helium neon laser/Evans blue
technique eliminates the response to ACh but in E enriched mice the
response to ACh was unaffected by the injury. More prolonged exposure
of the laser induces platelet adhesion/aggregation at the injured
site. A significantly longer exposure to the laser was required to
initiate adhesion/ aggregation in E enriched mice. Since effects of
endothelial damage in this model are mediated at least in part by
singlet oxygen produced by injured tissue (16) we conclude that the
antioxidant, radical scavenging actions of vitamin E explain the
protective action of the E enriched diet. However, raising vitamin E
levels did not protect against putative adverse effects of normally
occuring oxidants.
Received 27 September 1995; accepted in final form 19 December
1995.
APS Manuscript Number H912-5.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 22 January 96