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Inactivation of exogenous surfactant in experimental respiratory failure induced by hyperoxia
Author(s) -
Ennema J. J.,
Kobayashi T.,
Robertson B.,
Curstedt T.
Publication year - 1988
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.1988.tb02805.x
Subject(s) - medicine , hyperoxia , pulmonary surfactant , respiratory system , respiratory failure , intensive care medicine , anesthesia , lung , biochemistry , chemistry
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 PaO 2 was < 15 kPa or the PacO 2 > 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 (γ min ) close to zero. However, the γ 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.