Dependentatelectatic lung areas open towards the end of inspiration when the lungopening pressure increases, and recollapse during expiration. Wehypothesized that inhaled nitric oxide (NO) counteracts hypoxicvasoconstriction in these collapsing lung areas, resulting in increasedpulmonary shunt perfusion. We administered NO as apulse and varied the pulse timing during inspiration in equine anaesthesia, where atelectasis develops regularly. Six spontaneously breathing standardbreed trotters were studied under isoflurane anaesthesia in lateralrecumbency. NO pulsed into the first 30% of inspiration (group NOp1)was assumed to affect open lung areas. To cover more open lung areas NO wasthen pulsed into the first 60% of inspiration (group NOp2). In athird group, administration between 50 and 80% of inspiration wasaimed at the intermittently opening lung areas (groupNOp3). With NOp1, venous admixture decreased by 8(2)% (mean (sem), P=0.045) and with NOp2by 10 (1)% (P=0.01). With NOp3, venous admixturereduction was insignificant. Pulsedadministration of NO in early inspiration is optimal in reducing right toleft vascular shunt in atelectatic equine lung. This reduction ispositively correlated with the magnitude of the initial shunt. Withadministration in early inspiration, NO is mostly taken up by the lung. This prevents NO accumulation and NO2 formation in rebreathingcircuits. These findings may be important in humans when atelectasis occursincreasingly with overweight and age during anaesthesia, but also inpostoperative intensive care and in ARDS.