Normocarbic hyperventilation fails to induce pulmonary vasodilation.

The pulmonary vasodilator effect of increased rate of mechanical ventilation, with and without respiratory alkalosis, was studied in chronically instrumented newborn lambs. Pulmonary hypertension was first induced by ventilating with a hypoxic gas mixture. Subsequent respiratory alkalosis caused significant decreases in pulmonary arterial pressure and pulmonary vascular resistance. When normocarbia was re-established by adding carbon dioxide to the inspired gas, with the ventilator rate being held constant, the pressure and resistance returned to the baseline hypertensive state. Therefore, mechanical factors, either direct or indirect, appear to be of minor importance in the mechanism of pulmonary vasodilation secondary to frequency-induced hyperventilation.