Intracoronary nitroglycerin (NTG) increases coronary blood flow and NTG inhibits thromboxane (Tx) A2 production and release. However, whether an alteration in TxA2 is the mechanism by which NTG increases coronary blood flow is not known. Coronary sinus (CS) blood flow (BF) (by thermodilution) and the concentration of TxB2 (the stable metabolite of TxA2) in CS blood were measured in 23 patients (16 men and 7 women, aged 26 to 65 years) with coronary artery disease before, during and after injection of normal saline solution (n = 5, control subjects) or NTG, 100 μg (n = 18), into the left coronary artery. In the 5 control subjects, saline solution caused no change in CSBF or the concentration of TxB2 in CS blood. Ten of the 18 patients to whom NTG was given had received no cyclooxygenase inhibitors for 10 days. In these patients, NTG caused a marked increase in CSBF (from 112 ± 64 to 152 ± 70 ml/min, p <0.01) but no consistent change in the concentration of TxB2 in CS blood (141 ± 132 to 160 ± 155 pg/ml, difference not significant [NS]). The remaining 8 patients to whom NTG was given received aspirin before the study. In these patients, NTG caused a marked increase in CSBF (from 111 ± 39 to 180 ± 63 ml/min, p <0.01), even though the concentration of TxB2 in CS blood (8 ± 10 to 6 ± 6 pg/ml, NS) was lower (p <0.05) than that in control subjects and patients not receiving aspirin. Thus, although NTG induces a marked increase in CSBF, it exerts no effect on the concentration of TxB2 in CS blood, and its influence on CSBF is not affected by inhibition of TxA2 production and release. Therefore, the coronary vasodilatory action of NTG is not mediated by alterations in intracoronary TxA2.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine