Effects of inhaled nitric oxide in canine lung transplantation from non-heart-beating donor

Nitric oxide (NO) is believed to be identical to endothelium-dependent-relaxing-factor, a potent vasodilator. In addition, NO has been founded to play a critical role in the maintenance of vascular permeability through its attenuation of polymorphonuclear neutrophils (PMN) and platelets. In the present study, we have evaluated the effects of inhaled NO at reperfusion in canine left single-lung allotransplantation from a non-heart-beating donor. Twelve weight-matched pairs of adult mongrel dogs were used. The donor dogs were sacrificed by an intravenous injection of potassium chloride without heparinization. They were left at room temperature for 3 hours. Then, the recipient dogs received a left single-lung allotransplantation. After implantation, the right bronchus and pulmonary artery were ligated. In Group 1 (n = 6), NO gas was administered continuously at a concentration of 40 parts per million throughout a 6-hour assessment period. In Group 2 (n = 6), nitrogen gas was administered in the same manner as NO, for control. The survival time in Group 1 was significantly longer than that in Group 2. The arterial oxygen tension in Group 1 was significantly higher than that in Group 2. The pulmonary vascular resistance was significantly lower in Group 1 than in Group 2. The aortic pressure and the cardiac output each did not differ significantly between the two groups. Myeloperoxidase activity was significantly lower in Group 1 than in Group 2. Inhaled NO at reperfusion is beneficial in lung transplantation from non-heart-beating donors because it attenuates ischemia-reperfusion injury by inhibiting PMN activation and vasodilating pulmonary vasculature.