Abstract

Cardiac arrest (CA) remains a significant medical problem with stagnating low survival rates. Ventilation with the noble gas Argon (Ar) after return of spontaneous circulation improved neurologically favorable survival in a porcine CA model. We hypothesized that postconditioning with Ar attenuates global ischemia reperfusion (IR) injury in a rat isolated lung model. Following Institutional Animal Care and Use Committee approval and conforming with the "Position of the American Heart Association on Research Animal Use", lungs of adult male Sprague Dawley rats (250-350 g) were isolated and positive-pressure ventilated (10 mL/kg body weight [BW]) at a respiration rate of 30 breaths/minute. Lungs were perfused with physiological crystalloid buffer at a constant flow of 40 mL/kg BW. The control (C) group (n=6-7) was ventilated with 65% N 2 , 5% CO 2 , 30% O 2 , the Ar group (n=6) with 65% Ar, 5% CO 2 , 30% O 2 before global no-flow ischemia for 8 min followed by reperfusion. Mean arterial (MAP) and airway pressures (AWP) were recorded continuously. Lung viability as survival time until development of fulminant pulmonary edema was noted. Data are mean +/- SEM. Statistics: Student's t-Test with *p< 0.05. IR significantly increased MAP and AWP throughout reperfusion compared to baseline; contrary to our hypothesis, though, ventilation with Ar did not signficantly increase survival time (panel A) or lower MAP (B) or AWP (C) of the isolated lung during reperfusion in this model. In-vivo models may be better-suited to assess Ar’s organ-protective effects following CA.

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