Effects of L-arginine cardioplegia on myocardium

Abstract

Infusion of L-arginine (a precursor of nitric oxide, NO) in cardioplegia was examined to test its effect on metabolism of myocardium after myocardial ischemia and reperfusion (IR). Twenty-eight patients undergoing valve replacement were involved and randomly divided into two groups: the control group (crystalloid cardioplegia) and the experimental group (crystalloid cardioplegia + L-arginine). Blood samples were taken both before aortic clamping and after aortic unclamping from right radial artery to measure the concentrations of NO2-/NO3-, lactic acid (LA), malondialdehyde (MDA), superoxide dismutase (SOD), and xanthine oxidase (XOD). In the control group, the NO2-/NO3- level decreased at aortic unclamping, and 30 min later, it decreased significantly as compared with that before aortic clamping (p < .05). In the experimental group, it increased at aortic unclamping (p < .05), and 60 min later, increased to the peak. Five, fifteen, and thirty min after aortic unclamping, the concentrations of LA and MDA in the experimental group were lower than those in the control group (p < .05). Thirty and sixty min after aortic unclamping, the concentrations of SOD remained higher in the experimental group than those in the control group (p < .05). There was no difference between groups in the concentrations of XOD. The addition of L-arginine to the cardioplegia can protect the myocardium from injury by releasing nitric oxide.