Lung ischemia‐reperfusion injury stimulates airway biosensors through oxidative stress

Abstract

Lung ischemia‐reperfusion injury (LIRI) stimulates airway vagal chemosensors. We hypothesize that the stimulation is mediated by increased production of oxygen free radicals (OFRs). Two questions are asked: 1) Does increased production of OFRs by injecting a mixture of xanthine/xanthine oxidase into the receptive field stimulate airway chemosensors? 2) Can reduction of OFRs by intravenous infusion of superoxide dismutase (SOD) prevent LIRI induced chemosensor stimulation? Rabbits were anesthetized, the lungs were mechanically ventilated, the chest was opened, and airway chemosensor activities were recorded from the vagus nerve. LIRI was produced by closing (30 min) and then releasing (15 min) a snare around the pulmonary artery. Chemosensors activity increased sharply after local injection of xanthine/xanthine oxidase and peaked within 10 sec. The increased activity recovered within a min or so. The results demonstrate that the chemosensors are sensitive to increased OFRs. Chemosensor discharge (21±10 imp/min; baseline) increased to 56±36 imp/min (n=9; P=0.022) during the first min of reperfusion. Such increased activities after LIRI did not exist when SOD was infused intravenously for 20 min before reperfusion. Thus, antioxidants blocked the sensory response to LIRI. Our results support the hypothesis that LIRI activates airway chemosensors, which is mediated by increased production of OFRs.