Topical prostacyclin (PGI2) inhibits platelet aggregation in pial venules of the mouse.
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.
D000287:Administration, Topical; D000818:Animals; D001921:Brain / Q000098:blood supply*; D003864:Depression, Chemical; D011464:Epoprostenol / Q000008:administration & dosage / Q000494:pharmacology*; D008297:Male; D051379:Mice; D008813:Mice, Inbred ICR; D010974:Platelet Aggregation / Q000187:drug effects*; D011453:Prostaglandins / Q000494:pharmacology*; D014699:Venules
D011453:Prostaglandins; D011464:Epoprostenol