Rial arterioles were observed via direct microscopy or TV microscopy. Control mice were fed a "normal" diet with 55 lU/kg vitamin E (E) and were compared with either a group fed zero E or fed a high E diet (500 lU/kg). Even after 7 months on zero E there were no effects on the response of the arterioles to the topically applied, endothelium dependent dilator aoetylcholine (ACh) or on the ease with which local endothelial damage initiated platelet adhesion/ aggregation. 500 lU/kg failed to affect the response of normal arterioles to ACh but it prevented endothelial injury produced by a HeNe laser/Evans blue technique from abolishing the response to ACh. The laser/dye effects are caused in part by singlet oxygen produced by the injured vessel. More prolonged exposure to the laser causes adhesion/aggregation of platelets at the injured site. This took 50 ±11 sec (M±SD) in 10 control mica and 80±27sec (p<.01| in 10 supplemented mice. 500 IU/kg had no effect on aggregation in vitro using platelet rich plasma from the mice. Local adhesion/ aggregation in this model is modulated by EDRF/NO, an antiplatelet agent highly sensitive to oxidation and also the mediator of dilation produced by ACh. The present data shows no effect of dietary vitamin E on a response mediated by EDRF/NO in normal arterioles. But the effect, on EDRF/NO modulated responses, of an increased oxidative burden produced by the laser/ dye insult was ameliorated by elevated levels of antioxidant vitamin E.
|Published - 1996