Inhibition by prostacyclin of the tumor cell-induced platelet release reaction and platelet aggregation.
Prostacyclin was examined for its inhibitory effects on the tumor cell-induced platelet release reaction. Prostacyclin inhibited in a dose-dependent manner tumor cell-induced release of platelet dense granules and alpha-granules concomitant with an inhibition of platelet aggregation. Release was determined by assay of biochemical markers (serotonin for dense granules and beta-thromboglobulin for alpha-granules). A tenfold higher concentration of prostacyclin was required to inhibit completely serotonin release as compared to the concentration required for beta-thromboglobulin release. Correlative ultrastructural studies demonstrated that prostacyclin at doses of over 10 ng/ml inhibited the ultrastructural changes associated with tumor cell-induced platelet shape change and platelet granule release. Platelet aggregates exhibited the retention of granule reservoirs that could potentially be involved in long-term release of biologically active substances.
D000818:Animals; D001792:Blood Platelets / Q000187:drug effects* / Q000378:metabolism / Q000648:ultrastructure; D003594:Cytoplasmic Granules / Q000187:drug effects*; D011464:Epoprostenol / Q000494:pharmacology*; D051379:Mice; D008810:Mice, Inbred C57BL; D009362:Neoplasm Metastasis; D009374:Neoplasms, Experimental / Q000503:physiopathology*; D010974:Platelet Aggregation / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains
D011464:Epoprostenol