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.