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Ann Thorac Surg 1992;53:1033-1037
© 1992 The Society of Thoracic Surgeons
Department of Medicine, Leicester Royal Infirmary, and Department of Cardiothoracic Surgery Groby Road Hospital, Leicester, United Kingdom
Accepted for publication November 26, 1991.
* Address reprint requests to Dr Thurston, Department of Medicine, Clinical Sciences Building. Leicester Royal Infirmary, PO Box 65, Leicester LE2 7LX, United Kingdom.
The internal mammary artery has become the conduit of choice for coronary artery bypass grafting. Intraluminal papaverine treatment during operation reduces vasospasm and facilitates anastomosis. However, it has been suggested that papaverine may cause intimal damage, and accordingly we have investigated endothelial damage by comparing the responsiveness of internal mammary arteries before and after intraluminal exposure to papaverine (15 mg/mL). Control and papaverine-treated segments of internal mammary artery were obtained from 13 patients undergoing coronary artery bypass grafting and mounted as ring preparations in an organ bath. Cumulative dose contractions to noradrenaline were performed, and the dose producing a half maximal response was determined. Relaxation studies of submaximally contracted arteries were performed using the endothelium-dependent vasodilators acetylcholine and bradykinin and the endothelium-independent vasodilator sodium nitroprusside. In the human internal mammary artery the use of intraluminal papaverine increased the lumen size by 20% (p < 0.05), and the contractions elicited by noradrenaline were significantly less in the papaverine group than in the control group (p < 0.05). Endothelium-dependent relaxation to acetylcholine or bradykinin was not affected by papaverine treatment. Endothelium-independent relaxation was the same in both groups, with almost 100% relaxation achieved by sodium nitroprusside. These results indicate that intraluminal papaverine treatment during coronary artery bypass grafting causes a reduction of smooth muscle contraction and does not impair endothelium-dependent relaxation.
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