ABSTRACT
BACKGROUND: We investigated effects of platelets and prostacyclin formation in human internal mammary (IMA) and radial (RA) arteries. METHODS: IMA and RA segments were suspended in organ bath with increasing concentrations of platelets. Experiments were applied with and without ketanserin, a 5HT2 receptor antagonist, or U3405, a TXA2 receptor antagonist. The release of prostacyclin (PGI2) was assessed by enzyme immunoassay in vessels without endothelium, before and after contraction with angiotensin (AT) I-II. RESULTS: In IMA and RA with endothelium, platelets caused contractions, significantly enhanced in arteries without endothelium. Contractions to platelets were higher in RA than in IMA. U3405 reduced the platelet induced contractions in RA but not in IMA. Ketanserin inhibited the platelet induced contractions in IMA and RA. The basal release of PGI2 was more important in IMA than in RA. Addition of AT/I-II significantly reduced the release of PGI2 in IMA but not in RA. CONCLUSIONS: The RA responds more powerfully to platelets than IMA. Protective system with PGI2 seems to be more powerless in RA than in IMA. This accentuates the importance of antispastic and antiplatelet drugs when arteries are used for coronary artery bypass surgery.
