Adult guinea pigs were exposed to 100% oxygen until, after 54-85 h, they developed severe respiratory insufficiency. One subgroup of animals was ventilated artificially with 100% oxygen for an additional 60-960 min. When the PaO2 was less than 15 kPa or the PaCO2 greater than 20 kPa, 1 ml of porcine surfactant (phospholipid concentration 80 mg.ml-1) was instilled via the trachea. These animals were ventilated for one more hour and then sacrificed. Surfactant instillation did not improve the blood gases, nor the pulmonary pressure-volume characteristics. All hyperoxia-exposed guinea pigs showed prominent histologic lung lesions, including intraalveolar edema and desquamation of airway epithelium. Compared to normal guinea pigs the volume density of intraalveolar "gas" was decreased and that of intraalveolar fluid increased. The alveolar expansion pattern in histologic sections was not improved in the surfactant-treated animals, compared to hyperoxia-exposed guinea pigs studied immediately after death. In hyperoxia-exposed animals, about 1.5 ml of edema fluid was sampled from the airways. Evaluated with pulsating bubble, our surfactant preparation had a minimum surface tension (gamma min) close to zero. However, the gamma min values of edema fluid from surfactant-treated and nontreated guinea pigs were both about 20 mN.m-1. the edema fluid thus seemed to inhibit the essential physical properties of exogenous surfactant. This, together with the prominent lung lesions, may explain the failure of surfactant replacement therapy at a late stage of hyperoxia-induced respiratory failure.

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Lung-surfactant-deficient rabbits (n = 6) requiring artificial ventilation were subjected to a weaning-off regimen following surfactant replacement therapy. Surfactant-deficient rabbits (n = 6) that did not receive surfactant but underwent the same procedure served as controls. All surfactant-treated rabbits survived (i.e., reestablished spontaneous air breathing) whereas all the control animals died. In the surfactant-treated animals lung function improved in such a way that during the weaning period PaCO2 did not increase and the level of PaO2 remained significantly higher than in the control animals. The static lung compliance and the stability and expansion indices in vitro were significantly higher in the surfactant-treated rabbits. The lamellar body fraction of the lungs of surfactant-treated animals contained a significantly higher amount of surfactant phospholipids than those of the control animals. It is concluded that the animal model used in this study is an excellent tool for testing early effects of different surfactant preparations.

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