Experimental study on active oxygen species to warm ischemic lung. - Availability of GSH, SOD, and alloprinol -

Ischemic-reperfusion injury caused by oxygen-drived free radicals is one of the great problems to be solved for successful lung transplantation and preservation. This study was performed to clarify the effect of the free radical scavenger, reduced glutathione (GSH), superoxide dismutase (SOD), and alloprinol for warm ischemic lung, and to elucidate changes of active oxygen species production in neutrophils. Sixty-three mongrel dogs underwent hilar stripping following left thoracotomy. The left pulmonary artery, pulmonary vein, and left main bronchus were clamped for 2-3 hours. To reduce the free-oxygen radicals, alloprinol (30mg/kg /day, for 3 days peros), GSH (50mg/kg, I. V.) administration and perfusion through the pulmonary. artery with 4℃ Euro-Collins'solution including GSH(1mg/l), SOD (15mg/ml), and alloprinol (20mg/l) were performed. At the time of right pulmonary artery occlusion test, the blood gas analysis of arterial blood and measurement of left pulmonary arterial pressure were done on the pre-ischemic period, immediately after and one hour after declamping. At the same time, active oxygen species production in neutrophils was evaluated using flow cytometric procedure. 1) The good pulmonary gas-changing function remained after ischemic period by administration and perfusion with free radical scavenger GSH, SOD, and alloprinol. 2) Changes of pulmonary arterial pressure at right pulmonary artery occulision test was not statistically significant. 3) Production of active oxynene species in neutrophils was increased after ischemic period. In conclusion, all of GSH, SOD, and alloprinol are effective in elminating ischemia- reperfusion injury to warm ischemic lung