Air trapping and alveolar hyperinflation may occur during mechanical ventilation in the presence of severe airway obstruction, during fast ventilator rates, and when expiratory time is compromised. Inadvertent positive end-expiratory pressure may occur with air trapping and increased mean airway pressure. The pulmonary artery pressure response to air trapping, produced during volume-regulated time-cycled ventilation, was studied in neonatal lamb lungs, isolatedin situ, and perfused at a constant flow rate (50–75 ml.kg-1min-1), both before and after Ca2+-channel blockade with verapamil (5 mg). The hub of the endotracheal tube was narrowed to a 1.5-mm orifice to produce fixed proximal airway obstruction. Air trapping was then produced by lengthening inspiratory time from 25 to 80%, at zero end-expiratory pressure. The magnitude of inadvertent positive end-expiratory pressure due to air trapping was estimated by end-expiratory occlusion pressure. End-expiratory occlusion pressure was 0.20 ≤ 0.03 kPa (1.7 ≤ 0.2 mm Hg) and 1.60 ≤ 0.01 kPa (11.8 ≤ 1.0 mm Hg), at 25 and 80% inspiratory times, respectively. On lengthening inspiratory time, mean pulmonary artery pressure (mPpa) increased briskly within 30 s followed by a gradual increase over the next 4 min. Verapamil blunted both the brisk and the gradual increase in mPpa on lengthening inspiratory time. Lengthening inspiratory time increased the mPpa by 2.0 ≤ 0.1 kPa (14.7 ≤ 0.8 mm Hg) from baseline, and verapamil reduced this increase to 1.3 ≤ 0.1 kPa (10.1 ≤ 0.6 mm Hg; p < 0.05 by analysis of variance). Verapamil did not affect changes in mean airway and peak inspiratory airway pressures and the magnitude of inadvertent positive end-expiratory pressure caused by lengthening inspiratory time. In the neonatal lamb, the Ca2+-channel-dependent portion of the mPpa response to air trapping amplifies the Ca2+-channel-independent portion, which represents the compressive effects of airway pressure on the pulmonary circulation.