Introduction: Ventilation with the noble gas Argon during cardiopulmonary resuscitation (CPR) improved hemodynamics and demonstrated an antiarrhythmic effect in a porcine model of cardiac arrest.
Hypothesis: Ventilation with Argon has a Nitric Oxide (NO)-dependent vasodilatory effect on the pulmonary vasculature allowing more right-to-left-flow during CPR.
Methods: We isolated lungs from 8-week old Brown Norway rats and positive-pressure ventilated them with 10 mL/kg body weight. Both the pulmonary artery (PA) and the left atrium were cannulated for in- and outflow, respectively, and lungs were perfused at constant flow of 40 mL/kg body weight with a 4% Albumin Physiological Saline solution. During 30 min stabilization and for an additional 60 min of measurements, the lungs were ventilated with a 30% O2, 65% N2, 5% CO2 gas mixture. Ventilation was then switched for 60 min to 30% O2, 65% Argon, 5% CO2, followed by 20 min with 30% O2, 65% N2, 5% CO2. This was repeated in the presence of 100 μM of the non-specific NO synthase inhibitor NG-nitro-L-arginine methyl ester (LNAME). PA pressures and pulmonary flows were recorded for the duration of the study. Data are % baseline ± SEM. Statistics: ANOVA for repeated measures; P<0.05 (two-tailed) *vs Argon, †vs Argon&LNAME; n = 5.
Results: We observed a significant and completely reversible decrease in PA pressure (66±5%) when ventilating with Argon versus N2before (*91±5%) and after the switch (*91±6%). LNAME (*†100±9%) abolished the observed effect by Argon (87±4%).
Conclusions: Ventilation with Argon reversibly decreases pulmonary vascular resistance by 27% through a NO synthase-dependent mechanism. Argon-induced pulmonary vasodilation helps explain the observed increase in cardiac output during CPR in vivo.