Influence of organotins on rat platelet aggregation mechanisms.
The effects of ten organotins on rat platelet aggregation mechanisms were examined. Bis(tri-n-butyltin)oxide was the most potent inhibitor of both ADP- and collagen-induced aggregation, and it was the only organotin that directly induced aggregation. It also increased the latent period for induction of aggregation by collagen. Triphenyltin hydroxide was a weak inhibitor of both ADP- and collagen-induced aggregation. However, in contrast to bis(tri-n-butyltin)oxide, it decreased the latent period for collagen-induced aggregation. A similar effect also was observed with diphenyltin dichloride, phenyltin trichloride, and cyhexatin. Tri-n-butyltin chloride and tetra-n-butyltin demonstrated specificity in their action since aggregation induced by ADP but not collagen was inhibited. Tri-n-propyltin chloride, trimethyltin chloride, and fenbutatin oxide were without discernible effect on rat platelet aggregation.
D000244:Adenosine Diphosphate / Q000037:antagonists & inhibitors; D000818:Animals; D003094:Collagen / Q000037:antagonists & inhibitors; D066298:In Vitro Techniques; D008297:Male; D009947:Organotin Compounds / Q000633:toxicity*; D010974:Platelet Aggregation / Q000187:drug effects*; D051381:Rats; D011919:Rats, Inbred Strains
D009947:Organotin Compounds; D000244:Adenosine Diphosphate; D003094:Collagen; C007567:triphenyltin hydroxide