Absence of L-arginine effect on coronary hypersensitivity to serotonin in cardiac transplant recipients

Coronary hypersensitivity to serotonin promotes platelet aggregation and, t herefore, the progression of the atherosclerotic process. This abnormality occurs in the early stages of coronary atherosclerosis when the responses t o bradykinin are still preserved. To determine whether such changes also oc cur early after cardiac transplantation, intracoronary injections of bradyk inin and serotonin were performed in 7 control patients, in 19 patients wit h dyslipidemia, and in 15 cardiac transplant recipients (1 year after opera tion), Coronary angiography was normal in the 3 groups. In the segments whe re serotonin effects were the most pronounced, the diameter changes were me asured hy quantitative angiography. Bradykinin (60, 200, and 600 ng) increa sed in the same way as the coronary diameters in the 3 groups; in contrast, serotonin elicited vasodilation only in the control group (7 +/- 3%, perce ntage of baseline) and vasoconstriction in the hyperlipidemic group (-9 +/- 2%) and in transplant recipients (-15 +/- 3%). After intracoronary infusio n of L-arginine (40 mg/min for 14 minutes), serotonin-induced constriction was attenuated in the hyperlipidemic group hut not in transplant recipients . Thus, the response to bradykinin is preserved in the early stages of graf t vasculopathy, However, in contrast to patients with hyperlipidemia, the a bsence of an L-arginine effect on the responses to serotonin suggests the i nvolvement of mechanisms other than a decrease in endothelium-derived nitri c oxide availability. Immune processes promoting the release of endothelium -derived contracting factors such as endothelin and/or superoxide anion may play a role. (C) 1999 by Excerpta Medica, Inc.