Acetylcholine-Induced Endothelium-Dependent Responses in the Internal Mammary Artery and Grafted Saphenous Vein in Humans(in Vivo)

摘要

Background Coronary artery bypass grafts obtained from internal mammary artery(IMA) have a greater patency rate than do saphenous vein grafts(SVG). The release or production of endothelium-derived relaxing factor(EDRF), which regulates blood flow and inhibits platelets function, may contribute to the higher patency rate of IMA. In order to evaluate the difference between endothelium dependent relaxation in IMA and in grafted saphenous veins, we observed acetylcholine responses of IMAs and SVGs in humans. Method Incremental dose if acetylcholine(Ach:A1-20, A2-50, A3-100μg) or single dose if acetylcholine(A3) were infused into the non-grafted IMA in 16 patients with different clinical presentation of coronary artery disease(3 with stable angina, 2 with acute myocardial infarction 4 with variant angina and atypical chest pain syndrome in 7). After the dose-response to Ach was completed nitroglycerine 200μg was injected into the IMA. Graded dose of Ach (A1, A2, A3) was also infused in 13 grafted saphenous veins(SVG). Results The overall vascular effects of Ach into the IMA were dilatory responses regardless of different clinical presentation. Two or 3 minutes after Ach injection, the diameter of IMA increased by 9.2%(A1) and 16. 7%(A3) respectively(p Conclusion Injection of Ach to IMA and angiographically normal segments of SVGs caused vascular dilatation probably due to EDRF response. However the degree of relaxation was more prominent in IMA than in SVG. Angiographically diseased segments of SVGs had no response to Ach injection, suggesting that diseased SVG does not produce EDRF. However the finding of a consistent Ach-induced EDRF relaxation in the SVGs despite of constrictive response in the majority of native coronary arteries might suggest that the regenerated endothelial cell in the SVGs were probably of saphenous vein origin rather than derived from the coronary arterial endothelium.