L-arginine inhibits ischemia-reperfusion lung injury in rabbits

Background. Recent studies have reported that nitric oxide (NO) acts as a c ytoprotective mediator in ischemia-reperfusion (IR) lung injury. We hypothe sized that the addition of L-arginine to the perfusate would attenuate the increases in microvascular permeability and pulmonary vascular resistance. Materials and Methods. Isolated rabbit lungs were reperfused for 60 min aft er 120 min warm ischemia. Lung injury was assessed using the fluid filtrati on coefficient (K-f), pulmonary vasucular resistance (PVR) before ischemia and after reperfusion, and a wet-to-dry lung weight ratio (W/D). Results. The K-f of the control group (without L-arginine) was significantl y increased after reperfusion. Lungs perfused with L-arginine showed attenu ation of the IR-induced increases in K-f and PVR. Addition of N-omega-nitro -L-arginine (L-NA), a NO synthase inhibitor, to the perfusate reduced the b eneficial effects of L-arginine. The lungs perfused with dibutyrylcyclic GM P (dbcGMP) showed attenuation of IR-induced increases in K-f and PVR. There were no significant differences in the W/D ratio between these groups. Conclusions. These results demonstrate that L-arginine has beneficial effec ts on IR lung injury, perhaps due to enhancement of endothelial cGMP levels . (C) 1999 Academic Press.