L-arginine infusion dilates coronary vasculature in patients undergoing coronary bypass surgery

Abstract

Background: Nitric oxide-dependent factors (serotonin, activated platelets, acetylcholine) cause vasodilation in normal coronary arteries but vasoconstrict atherosclerotic vessels. This experiment tested the hypothesis that intravenous systemic infusions of L-arginine, a precursor for nitric oxide production, dilate the coronary vascular bed of patients undergoing coronary artery bypass graft surgery. Methods: Twenty patients scheduled for coronary artery bypass graft surgery surgery were studied in a prospective, blinded, randomized clinical trial. Saphenous vein graft blood flow was measured with a transit time flow probe, and coronary vascular resistance was calculated. After weaning from bypass, patients were given a venous infusion (placebo or 10% arginine hydrochloride [30 g]) over 15 min. Arterial blood samples for the determination of L-arginine and L-citrulline levels were drawn before, 10 min after starting infusion, and 10 min after end of infusion. Results: The placebo group experienced an increase in mean arterial pressure and coronary vascular resistance and a decrease in graft blood flow. Patients in the L-arginine group maintained their baseline values. Mean arterial pressure (Larginine, 88 ± 17 to 92 ± 13 mmHg vs. placebo, 80 ± 12 to 92 ± 9 mmHg, P = 0.021), coronary vascular resistance (L-arginine, 97,000 ± 60,000 to 99,600 ± 51,000 dynes · s · cm-5 vs. placebo, 81,000 ± 69,000 to 117,000 ± 64,000 dynes · s · cm-5, P = 0.05), and graft blood flow (L-arginine, 55 ± 25 to 50 ± 19 ml/min vs. placebo, 60 ± 34 to 46 ± 18, P = 0.05) remained more stable in the L-arginine-treated patients. Conclusions: Systemic L-arginine infusion reduced postby-pass coronary vasoconstriction. There were no adverse events associated with the drug infusion.