Effect of inhaled nitric oxide on experimentally induced pulmonary hypertension in neonatal foals

To evaluate the efficacy of inhaled nitric oxide (NO) in anesthetized healthy newborn foals with experimentally induced pulmonary hypertension.

Five 1- to 3-day-old foals.

Anesthesia was induced and maintained with propofol, and foals were intubated and mechanically ventilated. Systemic pressure and pulmonary arterial pressure (P(PA)) were recorded every 30 seconds. Hypertension was induced via a hypoxic gas mixture or chemical vasoconstriction, using the thromboxane mimetic U46619. Nitric oxide was added at a concentration of 80 parts per million (ppm) for 6 minutes under baseline conditions and during pulmonary hypertension-induced alveolar hypoxia (inspired oxygen concentration = 0.08). Nitric oxide (20, 40, 80, and 160 ppm) was evaluated during U46619-induced hypertension. Samples for determination of arterial blood gas tensions were collected before and after each NO treatment.

Inhaled NO (approx 80 ppm) did not have an effect on baseline variables. Infusion of U46619 (0.35 +/- 0.04 microg/kg of body weight/min) or alveolar hypoxia resulted in increased P(PA) and decreased arterial oxygenation (PaO2) and hemoglobin saturation (HbSat). The increase in P(PA) was attenuated, in a dose-dependent manner, by NO during U46619 infusion and reversed by NO during induced hypoxemia. The PaO2 and HbSat were significantly improved at all NO doses during U44619 infusion but not during alveolar hypoxia. For all inhaled NO concentrations, nitrogen dioxide and methoglobin values were < 5 ppm and 3%, respectively.

Nitric oxide is a potent, selective vasodilator of the pulmonary circulation in healthy newborn foals. Inhaled NO may have value as a therapeutic agent in foals with pulmonary hypertension.