Artificial surfactant therapy in hyaline-membrane disease

Using adult guinea-pigs, we have developed an experimental model in which alveolar surfactant phospholipids are removed by repeated lung lavage in vivo, and in which the short-term survival of the animals is ensured by artificial ventilation. Blood gases, parameters of lung mechanics, and histologic and electron microscopic findings indicate that the lavage procedure induces a condition similar to the adult respiratory distress syndrome. We propose that our technique might be used for evaluation of pharmacological agents and various forms of artificial ventilation which have been suggested for treatment of this disease.

In vivo lung lavage as an experimental model of the respiratory distress syndrome.

A borderline viability model of bronchopulmonary dysplasia (BPD)/chronic lung disease of infancy (CLD) with pathophysiologic parameters consistent with those in extremely immature humans with BPD/CLD is described. After prenatal steroid treatment of pregnant dams, 12 premature baboons were delivered by cesarean-section at 125 d (term gestation, 185 d), treated with exogenous surfactant, and maintained on appropriate oxygen and positive pressure ventilation for at least 1 to 2 mo. In spite of appropriate oxygenation (median Fi O2 at 28 d = 0.32; range, 0.21 to 0.50) and ventilatory strategies to prevent volutrauma, the baboons exhibited pulmonary pathologic lesions known to occur in extremely immature humans of less than 1,000 g: alveolar hypoplasia, variable saccular wall fibrosis, and minimal, if any, airway disease. The CLD baboon lungs showed significantly decreased alveolization and internal surface area measurements when compared with term and term + 2-mo air-breathing controls. A decrease in capilla...

https://www.atsjournals.org/doi/pdf/10.1164/ajrccm.160.4.9810071

Neonatal Chronic Lung Disease in Extremely Immature Baboons

Bronchopulmonary dysplasia: clinical presentation.

Bronchopulmonary dysplasia: changes in pathogenesis, epidemiology and definition

The pathologic changes in the lungs of 112 infants dying from hyaline membrane disease (HMD) and 64 infants dying from other causes in the years 1967 to 1972 have been reviewed in order to obtain information about the pathogenesis of bronchopulmonary dysplasia (BPD). The results from the infants with HMD showed that: a) From the fourth or fifth day, the surface tension of lung extracts fell, inclusion bodies became more plentiful, and air saccules with patent airways could be inflated with air, even when severe changes due to BPD were present. b) There was a highly statistically significant correlation between the most serious lesions of BPD--damage to airways followed by excessive repair and fibrosis--and the use of high (greater than 35 cm H2O) peak airway pressures during mechanical ventilation in life. c) Damage due to oxygen breathing could not be reliably identified although some of the lesions, particularly edema and fibroplasia in intersaccular septa, may have been caused by oxygen. d) Evidence of pulmonary hypertension was present in infants surviving for more than a month with severe lung damage, and the ductus arteriosus was always open. We conclude that the most important factor in the pathogenesis of BPD following HMD is mechanical trauma to the lung from the use of excessively high peak airway pressures during mechanical ventilation.

E. O. Reynolds

Papers

Pathogenesis of bronchopulmonary dysplasia following hyaline membrane disease.