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L-arginine inhibits ischemia-reperfusion lung injury in rabbits
K Yoshida1, K Yoshimura, M Haniuda
1Department of Surgery, Shinshu University School of Medicine, 3-1-1 Asahi, Matsumoto, 390, Japan.
Background:
Recent studies have reported that nitric oxide (NO) acts as a cytoprotective mediator in ischemia-reperfusion (IR) lung injury. We hypothesized 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 after 120 min warm ischemia. Lung injury was assessed using the fluid filtration coefficient (Kf), pulmonary vasucular resistance (PVR) before ischemia and after reperfusion, and a wet-to-dry lung weight ratio (W/D).
Results:
The Kf of the control group (without L-arginine) was significantly increased after reperfusion. Lungs perfused with L-arginine showed attenuation of the IR-induced increases in Kf and PVR. Addition of Nomega-nitro-L-arginine (L-NA), a NO synthase inhibitor, to the perfusate reduced the beneficial effects of L-arginine. The lungs perfused with dibutyryl-cyclic GMP (dbcGMP) showed attenuation of IR-induced increases in Kf and PVR. There were no significant differences in the W/D ratio between these groups.
Conclusions:
These results demonstrate that L-arginine has beneficial effects on IR lung injury, perhaps due to enhancement of endothelial cGMP levels.