Acute
alkalosis-induced pulmonary vasodilation and
acidosis-induced pulmonary vasoconstriction have been well described, but responses were generally measured within 5-30 min of changing pH. In contrast, several in vitro studies have found that relatively brief periods of sustained
alkalosis can enhance, and sustained
acidosis can decrease, vascular reactivity. In this study of intact newborn piglets, effects of acute (20 min) and sustained (60-80 min)
alkalosis or
acidosis on baseline (35% O2) and hypoxic (12% O2) pulmonary vascular resistance (PVR) were compared with control piglets exposed only to eucapnia. Acute
alkalosis decreased hypoxic PVR, but sustained
alkalosis failed to attenuate either baseline PVR or the subsequent hypoxic response. Acute
acidosis did not significantly increase hypoxic PVR, but sustained
acidosis markedly increased both baseline PVR and the subsequent hypoxic 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 accentuated during sustained
acidosis and after the resumption of eucapnia in
alkalosis-treated piglets. Although extrapolation of data from normal piglets to infants and children with
pulmonary hypertension must be done with caution, this study suggests that sustained
alkalosis may be of limited efficacy in treating acute
hypoxia-induced
pulmonary hypertension and the risks of
pulmonary hypertension must be considered when using
ventilator strategies resulting in permissive hypercapnic
acidosis.