It has long been claimed that the active expiratory glottic closure observed in newborns, especially during hyaline membrane disease, is related to hypoxia. However, we recently showed that hypoxia does not lead to active expiratory glottic closure in nonsedated lambs. In this study, we test the hypothesis that glottic closure is related to an excess of lung water present at birth. We studied 17 nonsedated lambs after inducing a permeability pulmonary edema via intravenous of either oleic acid (8 lambs) or halothane (9 lambs). We recorded airflow via a facial mask and pneumotachograph, as well as the electromyographic activity (EMG) of the thyroarytenoid muscle (TA), a glottic adductor. Blood gases were measured in 8 lambs via a brachial artery catheter. We identified laryngeal expiratory airflow braking on the breath-by-breath computed flow-volume loop and TA expiratory EMG as evidence of active expiratory glottic adduction. After the injection of oleic acid or halothane, an active expiratory glottic closure was recorded in all lambs but 1, usually throughout the recording period (60 to 300 min). The active expiratory glottic closure was not inhibited after correction of the hypoxia. We conclude that, in nonsedated lambs, a permeability pulmonary edema induces an active expiratory glottic closure. We hypothesize that the expiratory glottic closure commonly observed in newborns could help to ameliorate the alveolocapillary gas exchange by reopening the flooded alveoli.