1. Awake dogs with chronically implanted catheters (pulmonary artery, left atrium, aorta) and electromagnetic flow probe (main pulmonary artery) underwent five types of experiments in succession: (1) slow infusion of 0·4 m-hydrochloric acid; (2) rapid infusion of 1·0 m-sodium bicarbonate; (3) exposure to 30 min of hypoxia (10% O2); (4) exposure to hypoxia after arterial pH had been lowered to 7·30; (5) exposure to hypoxia after pH had been increased to 7·55. Intravascular pressures, pulmonary vascular resistance, cardiac output, arterial gas tension and pH were studied.
2. Acute acidosis (pH 7·21) resulted in a small rise in pulmonary artery pressure, cardiac output and pulmonary vascular resistance, associated with a decrease in Pa,co2. Acute alkalosis (pH 7·61) was accompanied by a small rise in pulmonary artery pressure, marked increase in cardiac output, a fall in pulmonary vascular resistance and mild elevation in Pa,co2. During acidosis hypoxia resulted in a more pronounced rise in pulmonary vascular resistance than during alkalosis (P < 0·01).
3. The study provides evidence that in the intact, awake dog with its compensatory mechanisms acute alkalosis decreases pulmonary vascular resistance by decreasing vascular tone and/or recruitment of pulmonary vascular channels; it diminishes the vasoconstrictive response to hypoxia; conversely, mild acidosis increases the pulmonary vascular resistance slightly and enhances vasoconstriction during hypoxia to a small extent.