Pulmonary vascular responses during acute and sustained respiratory alkalosis or acidosis in intact newborn piglets

Acute alkalosis-induced pulmonary vasodilation and acidosis-induced pulmona ry vasoconstriction have been well described, but responses were generally measured within 5-30 min of changing pH. In contrast, several in vitro stud ies have found that relatively brief periods of sustained alkalosis can enh ance, and sustained acidosis can decrease, vascular reactivity. In this stu dy of intact newborn piglets, effects of acute (20 min) and sustained (60-8 0 min) alkalosis or acidosis on baseline (35% O-2) and hypoxic (12% O-2) pu lmonary vascular resistance (PVR) were compared with control piglets expose d only to eucapnia. Acute alkalosis decreased hypoxic PVR, but sustained al kalosis failed to attenuate either baseline PVR or the subsequent hypoxic r esponse. Acute acidosis did not significantly increase hypoxic PVR, but sus tained acidosis markedly increased both baseline PVR and the subsequent hyp oxic response. Baseline PVR was similar in all piglets after resumption of eucapnic ventilation, but the final hypoxic response was greater in piglets previously exposed to alkalosis than in controls. Thus, hypoxic pulmonary vasoconstriction was not attenuated during sustained alkalosis, but was acc entuated during sustained acidosis and after the resumption of eucapnia in alkalosis-treated piglets. Although extrapolation of data from normal pigle ts to infants and children with pulmonary hypertension must be done with ca ution, this study suggests that sustained alkalosis may be of limited effic acy in treating acute hypoxia-induced pulmonary hypertension and the risks of pulmonary hypertension must be considered when using ventilator strategi es resulting in permissive-hypercapnic acidosis.