Abstract
A1-veloar hypoxia caused vasoconstriction in excised dog lobes studied with controlled perfusion and ventilation. Raising perfusate pH 0.2 units with tris (hydroxymethyl) aminomethane (THAM) or NaHCO3 eliminated the hypoxic constrictor response produced by an alveolar PO2 of 45 mm Hg. Re-establishment of the initial pH with lactic acid or HCE restored hypoxic reactivity. Graded degrees of hypocapnic alkalosis produced graded degrees of depression of the hypoxic pressor response. Restoration of the control pH with lactic acid during hypocapnia also restored the vascular responsiveness to hypoxia. Similar results were obtained using both blood and plasma perfusion. Changes in vascular reac -tivity were not the result of alteration of airway resistance or compliance. It is concluded that pH alterations over a range obtainable in pathologic states can profoundly affect any intrinsic pulmonary vascular adjustments that are responses to local O2 tension.