No effect of L-arginine supplementation on pulmonary endothelial dysfunction after cardiopulmonary bypass.

Abstract

Acetylcholine is an endothelium-dependent vasodilator through the L-arginine-nitric oxide pathway. After ischemia-reperfusion this effect is attenuated, also demonstrated in the pulmonary circulation after cardiopulmonary bypass. Administration of L-arginine has been shown to have a protective effect on endothelial function in reperfusion injury. The aim of the current study was to test the possible effect of L-arginine on the acetylcholine reactivity in the pulmonary circulation after cardiopulmonary bypass. Thirty-five patients with ischemic and/or valvular heart disease were investigated in a randomized, double-blinded, placebo-controlled study. The patients were divided into three groups. Group 1: high dose L-arginine (n=10), group 2: low dose L-arginine (n=10), group 3: placebo, no L-arginine, (n=15). The acetylcholine reactivity was tested with measurements of pulmonary vascular resistance before surgery and 1, 2 and 3-4 h after cardiopulmonary bypass. After cardiopulmonary bypass an attenuation of the acetylcholine reactivity over time was observed in all groups, with no differences between groups. In the current study L-arginine had no protective effect on the pulmonary endothelium after cardiopulmonary bypass, measured as reactivity to an infusion of acetylcholine.