Introduction: The most important issue in the success of coronary bypass surgery is the quality of the grafts used. In this study, the effect of vasodilator drugs for intimal damage on the harvested saphenous veins of coronary bypass patients was investigated. Patients and Methods: A total of 10 patients who underwent coronary bypass surgery, had 2-cm long segments of saphenous veins harvested and divided into four study groups. Isotonic solutions in Group I (control group) and Group II, verapamil in Group III, and nitroglycerin in Group IV were applied to the saphenous veins at equal times, in the control group under 20 mmHg and in the other groups 100 mmHg pressure. Upon the completion of the preparation, saphenous vein grafts were studied with light and electron microscopy. Endothelial cell loss and intimal and medial edema were considered in evaluations. Scoring was done from 0 to 3. A median score was assessed for each group. Results: There was a statistically significant difference between the control and saline groups in terms of endothelial and media damage (0.7 ± 0.48, 2.8 ± 0.42) (p< 0.001), while there was no statistically significant difference between the control group and the verapamil and nitroglycerin groups (0.7 ± 0.48, 1.4 ± 0.54) (0.7 ± 0.48, 1.2 ± 0.44) (p> 0.05). Likewise, no statistically significant difference was found between verapamil and nitroglycerin (1.4 ± 0.54, 1.2 ± 0.44) (p> 0.05). It was determined that the verapamil and nitroglycerin groups had the closest score to the control group, the endothelial and medial damage was minimal in the verapamil and nitroglycerin group, like the control group, and a large amount of endothelial and media damage was observed in the saline group. Conclusion: The use of vasodilators (verapamil or nitroglycerin) in the preparation of the saphenous vein graft increases the early and late success of vein grafts by protecting the tunica intima and media in the graft, preventing the formation of thrombus in the early period and the development of branchendothelial fibromuscular hyperplasia and atherosclerosis in the late period.