Internal Medicine

Download Lung Development and Regeneration (Lung Biology in Health by Donald J. Massaro, Gloria DeCarlo Massaro, Pierre Chambon PDF

By Donald J. Massaro, Gloria DeCarlo Massaro, Pierre Chambon

This reference compiles the most up-tp-date technical and organic information on hand to survey the state-of-science within the care and administration of sufferers with bronchopulmonary dysplasia, COPD, and different kinds of lung disease-tracking the initiation and development of techniques that reason airway obstruction, the biologic and physiological abnormalities that represent COPD, and the aptitude reversibility of the inflammatory reaction in COPD for greater sufferer analysis and therapy.

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Sample text

IV. Animal Models of Postsurfactant BPD Defining the pathophysiology of BPD in the postsurfactant era has been a formidable challenge and has relied to a large extent on the detailed observations made on authentic animal models of this condition. These have included chronic ventilation experiments conducted with prematurely delivered baboons at the Southwest Foundation in San Antonio, Texas (35–39), and similar studies with premature lambs mechanically ventilated for 3–4 weeks by the group in Utah (40–44).

Arrested alveolar development was documented quantitatively by low Emery counts of the terminal respiratory units. In those infants who lived 17–156 days, airway changes, such as squamous metaplasia and peribronchial fibrosis, were infrequent and negligible. Margraf, et al. examined autopsy specimens of 8 infants who were born at gestational ages of 24–30 weeks (birthweights were not given), had HMD, and died at postnatal ages of 2–28 months (20). Their lungs showed varying amounts of bronchial and bronchiolar squamous metaplasia, marked simplification of acinar structure, variable but constant alveolar septal fibrosis, and abnormalities in elastic fiber architecture and arrangement.

BPD in Postsurfactant Era 27 This analysis is complicated by the fact that survival of very premature infants who are at greatest risk of BPD has improved by as much as 30% since the advent of surfactant treatment. It might be argued, therefore, that the proper denominator for comparing the incidence of BPD in the various surfactant trials should be the number of surviving infants rather than the number of randomized infants. At least one epidemiological study that took this tack, however, did not find a significant difference between the incidence of BPD among surfactant-treated and untreated survivors (62).

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