Ventilation-perfusion mismatch after lung ischemia-reperfusion - Protective effect of nitric oxide

Lung ischemia-reperfusion provokes pulmonary hypertension and increased mic rovascular permeability with subsequent edema formation and hypoxemia. We e xposed buffer-perfused rabbit lungs to 120 and 180 min of warm ischemia. Af ter reperfusion, gas exchange disturbances were analyzed by the multiple in ert gas elimination technique (MIGET). Additionally, ischemic lungs were tr eated with different doses of inhaled nitric oxide (NO) throughout reperfus ion. Reperfusion provoked a transient pulmonary artery pressure elevation, followed by progressive pulmonary edema formation. After 120 min of ischemi a, severe ventilation-perfusion ((V) over dot A/(Q) over dot) mismatch deve loped within 15 min of reperfusion, with the appearance of low (V) over dot A/(Q) over dot areas and marked broadening of both perfusion and ventilati on distribution in the midrange (V) over dot A/(Q) over dot regions. In par allel, shunt flow increased from less than 2% to approximately 17%. Inhalat ion of NO suppressed the presser response, edema formation, as well as (V) over dot A/(Q) over dot mismatch and shunt flow. Concentrations of 10 and 5 0 ppm NO were equipotent, surpassing the efficacy of 1 or 250 ppm NO. Inhal ation of NO, however, did not protect from the overwhelming gas exchange an d fluid balance disturbances provoked by 180 min ischemia. In conclusion, s evere abnormalities in gas exchange occurred rapidly upon reperfusion of is chemic lungs. Prophylactic NO inhalation may be considered for maintenance of gas exchange in settings of ischemia-reperfusion including lung transpla ntation.