The Pulmonary Arteries and Arterioles in Hyaline Membrane Disease.

The pathogenesis of hyaline membrane disease is not only unsolved but also highly controversial and 'there exist almost as many theories about it as there have been serious observers' (Stowens, 1959). Among these theories some are based on the assumption that circulatory disturbances play a role in the development of the hyaline membranes. Transudation of constituents of blood plasma has been considered a factor in this process by many authors (Hadders and Dirken, 1955; Jarrett, 1957; van Breemen, Neustein and Bruns, 1957; Piper and Kleppe, 1958; Engelhardt, 1961). Alveolar capillary congestion and pulmonary oedema are commonly observed in lungs of infants with pulmonary hyaline membranes (Ziegler, 1957; Shanklin, 1959; Carone and Spector, 1960): this may be due to damage to the capillary wall resulting in increased capillary permeability. However, the exceedingly common, although not exclusive, association of hyaline membrane disease of the lung with prematurity has led some workers to believe that the lack of maturity of pulmonary tissue may play a role in such an increased permeability (Brummelkamp, 1958; Goebel, Koburg and Thelen, 1962). Others (O'Neal, Ahlvin, Bauer and Thomas, 1957) have noticed that the media of muscular pulmonary arteries and arterioles in premature infants is less well developed as compared to that in full-term newborns and suggested that this may be a factor in the development of hyaline membranes. Rudolph, Drorbaugh, Auld, Rudolph, Nadas, Smith and Hubbell (1961), who performed cardiac catheterization in a number of infants with hyaline membrane disease, suggested that there was decreased vasoconstrictive activity both in systemic and pulmonary circulation. In a quantitative study of the medial muscle mass of pulmonary arteries in foetuses and infants, one of us (Wagenvoort, Neufeld and Edwards, 1961) showed that normally there is a gradual increase in the amount of pulmonary arterial muscle tissue during foetal life, with a maximum at the time of birth. In other words, the media of pulmonary arteries and arterioles in premature infants is not yet fully developed. If this fact should in any way be related to the pathogenesis of hyaline membrane disease, we may expect that, on the average, infants with this form of respiratory distress should have a smaller arterial muscle mass than infants of similar gestational age without this disease. In this study we have compared the thickness of the media and the total amount of medial muscle tissue of premature infants having hyaline membrane disease with that in premature infants who died of other causes, in order to see if the pulmonary arteries in the first group differ in any respect from a normal control series.