PROSTACYCLIN (PGI(2)) INHIBITS THE FORMATION OF PLATELET THROMBI IN ARTERIOLES AND VENULES OF THE HAMSTER-CHEEK POUCH (REPRINTED FROM BRIT J PHARMACOL, VOL 63, PG 535-539, 1978)
Ea. Higgs et al., PROSTACYCLIN (PGI(2)) INHIBITS THE FORMATION OF PLATELET THROMBI IN ARTERIOLES AND VENULES OF THE HAMSTER-CHEEK POUCH (REPRINTED FROM BRIT J PHARMACOL, VOL 63, PG 535-539, 1978), British Journal of Pharmacology, 120(4), 1997, pp. 439-443
1 Isolated rings of hamster aorta produced an unstable substance which
inhibited platelet aggregation in vitro and had the same characterist
ics as prostacyclin. 2 Prostacyclin inhibited adenosine diphosphate (A
DP)-induced aggregation of hamster platelets in vitro. 3 The effects o
f prostacyclin on ADP-induced platelet thrombi in the microcirculation
of the hamster cheek pouch were studied with a television microscope.
4 Prostacyclin caused a dose-dependent increase in the time of iontop
horetic application of ADP which was required to induce platelet throm
bi formation and embolization in venules (30 to 40 mu m diameter). 5 P
rostacyclin caused a dose-dependent reduction in the total time during
which ADP-induced thrombi were observed following local electrical da
mage to arterioles (40 to 80 mu m diameter). 6 Thrombus formation in v
enules and arterioles was abolished by 500 ng/ml prostacyclin in the K
rebs solution superfusing the hamster cheek pouch. 7 Prostacyclin was
approximately twenty times more potent than prostaglandin E-1 in preve
nting thrombus formation in the microcirculation.