Long-term patency of coronary artery bypass grafts (CABG) with internal mammary artery (IMA) is better than with saphenous vein (SV) grafts. To determine if vascular prostacyclin (PGI2) produced by IMA might contribute to the improved outcome, we compared PGI2 generated by IMA and SV fragments from 26 patients undergoing CABG and tested the effect of preoperative, long-term ingestion of of aspirin. Fresh tissues were incubated in buffer +/- 25 mumol/L of sodium arachidonate at 37 degrees C for 5 minutes to stimulate PGI2 production, measured by radioimmunoassay of its major hydrolytic product, 6-keto-PGF1 alpha. Results were expressed in picograms of 6-keto-PGF1 alpha per milligram tissue wet weight for total PGI2 production by vascular segments and picograms per cm2 surface area for endothelial PGI2 production. Endothelial PGI2 production was compared for IMA and SV in template-stirring chambers that exposed only the luminal surface of the vessel, excluding underlying smooth muscle. Endothelial PGI2 production by IMA was significantly higher than production by SV under both basal (mechanical stimulation only 1436 +/- 224 versus 842 +/- 227 pg/cm2, mean +/- SEM, p greater than 0.05) and stimulated (25 mumol/L sodium arachidonate: 3343 +/- 347 versus 2032 +/- 465 pg/cm2, p less than 0.025) conditions in patients not receiving aspirin. For patients receiving aspirin, endothelial PGI2 production by IMA was significantly higher than production by SV in stimulated conditions (1382 +/- 526 versus 683 +/- 124 pg/cm2, p less than 0.05). Histologic examination of the tissue segments revealed intact endothelium after incubation in both IMA and SV. Thus a high capacity for PGI2 synthesis and diminished inhibition of PGI2 after aspirin were demonstrated for IMA compared with SV tissue and may be a factor in the improved patency of IMA grafts.