Abstract
Local application of prostacyclin (PGI2) to cerebral (pial) microvessels, inhibited the aggregation of platelets induced in the vessels by exposing them to a filtered mercury light source following intravenous sodium fluorescein. The inhibition was consistantly observed in venules rather than arterioles and was manifest by a lengthening of the time required for the noxious stimulus to produce an initial aggregate, and/or by a lengthening of the time required for enlarging aggregates to totally block the venule. The consistency of the inhibition diminished at doses below 100 microgram/ml. Inhibition was observed whether or not alcohol was used as the vehicle for PGI2 and whether or not the body temperature of the anesthetized mouse was permitted to fall.
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