ABSTRACT
Recent studies have demonstrated that nitric oxide (NO) acts as a pulmonary vasodilator when inhaled in low concentrations. Due to the physicochemical similarities between NO and carbon monoxide (CO), it was speculated that low concentrations of CO would have similar effects in the isolated rat lung. The purpose of this study was to determine the role of CO (200 and 1000 ppm) in modulating hypoxia- and angiotensin II (AII)-induced pulmonary vasoconstriction, using isolated salt-perfused lungs of normotensive (CON) or pulmonary hypertensive male rats. Pulmonary hypertensive rats (ALT), induced by simulated altitude exposure (4572 m; 430 mm Hg for 32-48 days), were studied to determine the actions of low-dose CO in a remodeled pulmonary vascular bed. Right ventricular hypertrophy and polycythemia were evident in the ALT rats, suggesting that simulated altitude exposure induced pulmonary hypertension and consequent pulmonary vascular remodeling. CO did not significantly affect pulmonary vascular responses to acute hypoxia (6% CO2, balance N2) in either CON or ALT rats. There were also no significant differences in pulmonary pressor responses to AII injections (0.2 or 0.4 micrograms) in CON or ALT lungs either immediately following or during an acute hypoxia + CO exposure. Therefore, acute low-dose CO exposure (< 1000 ppm) does not appear to attenuate pulmonary vasoconstriction in isolated rat lungs.
