P e d i a t . Res. 12: 249-255 (1978) Bronchiolar lesions n e w b o r n intermittent positive pressure respiratory distress s y n d r o m e ventilation (IPPV) bronchiolar epithelium, whereas such lesions were scarce or T , obtain the honlo~ogous surfactant suspension, we washed absent in surfactant-treated animals. Our findings indicate that the lungs of adult rabbits using a to an lung compliance of the premature neonate can be increased by endotrachcal cannula, ~h~ lavage fluid was first centrifuged at deposition of surfactant in the upper airways before the onset of 200 x g and 20" for 5 mi" to remove cellular contamination. ventilation, and that deposition of surfactant prevents the devel-then centrifuged at 1000 x and 40 for 1 hr, hi^ procedure opment of bronchiolar epithelial lesions in premature neonates yields a white in surpace-active phosp~olipids subjected to IPPV.(2). The pellets were resuspended in an equal volumc of supernatant. then pooled and frozen until used for deposition. SpeculationThe phospholipid content of the surfactant pool used in thc present experiments was 8.4 mg/rnl, the lecithin content 6.9 mg/ The possibility that administration of supplementary surfac-m l . tant might serve as a prophylaxis against RDS and against epithelial lesions induced by artificial ventilation should be further evaluated in animal experiments and the clinical appli-ARTIFICIAL VENTILATION O F FETUSES cation of analogous prophylactic measures considered, once ~h , experiments were carried Out on 1 6 premature fetuses, synthetic surfactant suspensions with optimal phospholipid (or obtained from 8 does. We killed the doe, 27 days less 1-3 hr phospholipid-protein) composition have been defined. after mating (full term = 31 t 1 day). by intravenous injection of 2 ml Mebumal (sodium pentobarbital. 6 0 rng/ml) and 5 ml potassium chloride (1 50 mg/ml). The abdomen was immediately The spcctruln of structural abnorrnalitics that characterize the opened, and the blood vcsscls of the uterus were c l a~i~p c d with lungs of infants dying from the neonatal RDS includes necrosis a large hemostat. The fetuses were delivered through random and dcsquamation of the bronchiolar epithelium (5,6,21). This uterine incisions and weighed. We used two fetuses from each feature, which is particularly prominent in very immature infants doe, one for deposition of surfactant and one serving as control. who die from RDS within a few hours after birth. is part of the Body weight in surfactant-treated animals ranged between 26"natural" course of the disease, i.e.,it is not restricted to patients and 34 g ( j ( = 31, S D = 3), and in controls between 27 and 3 8 receiving artificial ventilation. However, when a patient with g (k = 31. SD = 3). Within a few seconds after delivery the severe RDS develops the complication known as "bronchopulfetuses received an intraperitoneal injection of 0.6 mg Mebuman monary dysplasia," the degree of bronchiolar epithelial lesions and 0.02 mg Pavulon (pancuronium bromide). In order to appears to be cor...
Ten newborn infants (795-1680 g) with severe respiratory distress syndrome (RDS) were treated with the isolated phospholipid fraction of bovine or porcine surfactant, which was administered via the airways (dose 200 mg/kg), at a median age of 10.5 h. Before receiving surfactant, all the infants were on artificial ventilation (FiO2 0.6-1.0). Within 2 h after surfactant replacement, the arterial-to-alveolar PO2 ratio increased from 0.1 to 0.35. There was a concomitant improvement in lung aeration on the chest roentgenograms and a significant reduction in the right-to-left shunt. Four patients died of cerebral hemorrhage; two of them also had a patent ductus arteriosus. One surviving infant developed bronchopulmonary dysplasia, and another succumbed 8 months later to the sudden infant death syndrome. No antibodies against surfactant were detected in the sera of the survivors. Since our results show a significant improvement in lung function after replacement therapy, the efficacy of this new surfactant preparation should be further tested in randomized clinical trials.
ABSTRACT. Modified natural porcine surfactant was mixed with edema fluid sampled from the airways of hyperoxia-exposed adult rabbits. By varying the concentration of surfactant lipids (10, 25, and 50 mg/mL) and edema fluid proteins (0-280 mg/mL), we obtained a series of preparations with protein to surfactant lipid weight ratios ranging from 0 to 11.2. The surfactant activity of these various mixtures was analyzed with a pulsating bubble (at a lipid concentration of 1 0 mg/mL) or in experiments on immature newborn rabbits (at lipid concentrations of 25 or 50 mg/mL). For the latter purpose, animals were delivered at a gestational age of 27 d and ventilated with a standardized sequence of insufflation pressures after receiving 0.1 mL of the surfactant-edema sample into the airways a t birth. Nearly complete in vitro inhibition of surfactant (markedly delayed film adsorption and a minimum surface tension of 23 mN/m during pulsation) was observed at a protein to surfactant lipid ratio of 4.5. Under in vivo conditions, nearly complete surfactant inhibition (tidal volumes reduced to less than 20% of the values for littermates ventilated with the same pressure after receiving surfactant without admixture of edema fluid) was documented at a protein to surfactant lipid ratio of 11.2. Our data suggest that the functional properties of an immature neonatal lung, in which serum proteins tend to leak into the airspaces after the onset of ventilation, depend on the stoichiometric relation between surfactant lipids and inhibitory proteins in the lung liquid. (Pediatr Res 29: 353-356, 1991) Abbreviations P/L, protein to surfactant lipid Surfactant CK, modified natural porcine surfactant Respiratory distress syndrome of the premature newborn infant is the result of at least two pathophysiologic mechanisms. One is a deficiency of lung surfactant phospholipids and associated proteins, the other is a leakage of serum proteins into the airspaces (1). These two factors are intertwined, inasmuch as ventilation of surfactant-deficient lungs causes epithelial disrup-
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