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 c
oncentrations of platelets. Experiments were applied with and without ketan
serin, a 5HT(2) receptor antagonist, or U3405, a TXA(2) receptor antagonist
. The release of prostacyclin (PGI(2)) was assessed by enzyme immunoassay i
n vessels without endothelium, before and after contraction with angiotensi
n (AT) I-II.
Results. In IMA and RA with endothelium, platelets caused contractions, sig
nificantly enhanced in arteries without endothelium. Contractions to platel
ets were higher in RA than in IMA. U3405 reduced the platelet induced contr
actions in RA but not in IMA. Ketanserin inhibited the platelet induced con
tractions in IMA and PA. The basal release of PGI, was more important in IM
A than in RA. Addition of AT/I-II significantly reduced the release of PGI,
in IMA but not in RA.
Conclusions. The RA responds more powerfully to platelets than IMA. Protect
ive system with PGI, seems to be more powerless in RA than in IMA. This acc
entuates the importance of antispastic and antiplatelet drugs when arteries
are used for coronary artery bypass surgery. (C) 2000 by The Society of Th
oracic Surgeons.