The mechanism of nitrous oxide-induced changes in pulmonary vascular resistance in a dog model of left atrial outflow obstruction.

Nitrous oxide has been reported to increase pulmonary vascular resistance (PVR) in patients with pulmonary hypertension secondary to mitral stenosis. Additional data suggest this response involves sympathetic stimulation because the increase in PVR can be prevented by alpha-adrenergic and ganglionic blockade. Whether or not active pulmonary vasoconstriction occurs remains unclear. This study was designed to more fully characterize the influence of N2O on pulmonary hemodynamics during left atrial outflow obstruction (LAO). Responses in an in situ blood-perfused lung lobe were compared with those in the remaining intact lung of six dogs anesthetized with pentobarbital, 30 mg/kg, and morphine, 1.5 mg/kg, and prepared for measurement of peak left ventricular (LV) pressure, LV end-diastolic pressure (LVEDP), LV dP/dt, systemic arterial and pulmonary arterial (PA) pressures, and cardiac output (CO). The pulmonary artery branch supplying the left middle lung lobe was cannulated and perfused at a constant rate with warmed blood. LAO was produced by filling the balloon of a Foley catheter positioned in the left atrium (LA) with enough saline to increase PA pressure by 50%; the balloon was subsequently left filled for the entire protocol. Measurements were first obtained during ventilation with 67% N2, and 33% O2. The inspired gas was then changed to 67% N2O and 33% O2 for 10 minutes, and then returned to the N2/O2 mixture. Once baselines had been reestablished (about 10 minutes), phentolamine, 0.75 mg/kg, was administered, and the response to 10 minutes of N2O again observed. N2O did not change vascular resistance in the isolated lobe, but increased intact-lung PVR.(ABSTRACT TRUNCATED AT 250 WORDS)