Inhaled argon dilates pulmonary vasculature in rat isolated lungs.

During cardiopulmonary resuscitation, pulmonary vasoconstriction due to hypoxia and hypercarbia restricts blood flow from the right to the left heart, resulting in reduced cardiac output that further inhibits adequate oxygenation and the ability to distribute oxygenated blood and medications. An inhaled pulmonary vasodilator could attenuate vasoconstriction and, therefore, increase cardiac output. We used rat isolated lungs to test if inhaled Argon leads to pulmonary vasodilation in phenylephrine-treated lungs. Lungs of 13 adult male Sprague-Dawley rats were isolated, ventilated, and perfused. Pulmonary artery and left atrium were cannulated and lungs perfused at constant flow with 4% albumin physiological saline solution. Controls ( n  = 6) were ventilated with 65% N ₂ , 5% CO ₂ , 30% O ₂ , and Argon lungs ( n  = 7) with 65% Argon, 5% CO ₂ , and 30% O ₂ . Pulmonary mean arterial pressure (pMAP) and airway pressure (AWP) were recorded continuously, and pulmonary vascular resistance (PVR) was calculated. Following baseline readings, phenylephrine, a pulmonary vasoconstrictor, was perfused at increasing concentrations from 10 ^-7 to 10 ^-3  mol/L every 5 min. Statistics: Student's t test, α = 0.05. Argon led to significantly lower pMAPs and PVRs, independent of AWP. Thus, it significantly dilated pre-constricted pulmonary vessels in an ex vivo lung model. When given during resuscitation, this might aid to increase cardiac output.
Competing Interests: Dr. Riess is co-inventor of US patent US-10828436-B2 entitled “Administering the Noble Gas Argon During Cardiopulmonary Resuscitation”. No other conflicts of interest, financial or otherwise, are declared by the authors.