High-frequency oscillatory ventilation (HFOV) permits adequate gas exchange but avoids the large phasic pressure-volume excursions of conventional mechanical ventilation (CMV); such avoidance may reduce the lung injury associated with hyaline membrane disease (HMD). We hypothesized that premature monkeys ventilated from birth with HFOV would have reduced lung injury compared to those assigned to CMV. Macaca nemestrina were delivered at 134 days (80% of term gestation) and ventilated from the first breath with either HFOV (n = 10) or CMV (n = 10). The mean airway pressure (Paw) was kept at 15 cm H2O pressure in HFOV animals; in CMV animals Paw was increased from 8 cm H2O at 2 h to 13 cm H2O at 6 h to prevent hypoxemia. At the conclusion of the 6-h experiment the HFOV animals had better oxygenation (p less than 0.05) and less evidence of HMD by chest radiograph (p less than 0.05). At 6 h of age a piece of the right middle lung lobe was removed, divided, and placed in fixatives for light and transmission electron microscopy. The lungs were subsequently inflated to 30 cm H2O pressure, and the right lower lobe was rapidly frozen in situ for morphometric studies. The proportion of peripheral lung tissue occupied by clear alveoli was greater in HFOV animals (66.3 +/- 14.8%) than in those assigned to CMV (44.2 +/- 16.9%, p less than 0.01); less alveolar debris and fluid was present in the HFOV animals (12.7 +/- 9.9%) compared with CMV animals (27.1 +/- 12.5%, p less than 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
To investigate the relative toxicities of inhaled volcanic ash and quartz, we exposed matched groups of rats to either respirable volcanic ash (100 mg/m3), quartz (100 mg/m3), or clean air only for 6 h daily for 10 days. Thereafter, we examined animals sequentially for as long as 9 months, and measured changes in lung histopathologic aspects, air-space cells and lipids, and lung density. Neutron activation studies demonstrated that 3.3% of the inhaled daily dose of volcanic ash was detectable in the lung parenchyma. Volcanic ash was less toxic to the lung than quartz. Immediately after exposure, the lungs of animals treated with volcanic ash had ultrastructural evidence of damage to type I pneumocytes and early alveolar edema formation. By contrast, quartz-treated animals had an intense acute injury, with intraalveolar accumulation of lipid, protein, macrophages, and granulocytes. Six months after exposure, animals treated with volcanic ash had moderate interstitial thickening and fibrosis, whereas the quartz-treated animals had severe pulmonary fibrosis. Quartz, but not volcanic ash, caused a marked increase in lavage granulocytes, protein, and phospholipids. Lung density increased in quartz-exposed, but not in volcanic-ash-exposed animals. These data indicate that volcanic ash is less harmful to the lung parenchyma than is quartz. Persons exposed to volcanic ash for short periods are at much less risk of subsequent lung damage than are those who are exposed to similar amounts of quartz in the workplace.
SummaryThe biological and physiologic maturation of the lung in the primate M a c a c a nemestrina (pigtail monkey) from 1 0 7 days of gestation through term is the subject of this report. Total lung volume increased approximately 1CO% during the last 20% of gestation (Fig. 1). The increase from 30% to 85% of total lung volume a t a deflation pressure of 1 0 cm H,O indicates a marked change in lung stability during the last 30-40 days of gestation (Fig. 2). Lung phospholipid per g dry weight of lung more than doubles during the last 20% of gestation (Fig. 3). This increase in phospholipid is due almost entirely to a n increase in lecithin, and surface active material (SAM) lecithin accounts for the major part of this increase (Figs. 4 and 5). The increases in total lung and SAM lecithin parallel but precede the increase in lecithin in amniotic fluid (Fig. 6). A s lung SAM increases the amniotic fluid lecithin t o sphingomyelin ratio also increases ( Fig. 7 and Table 1). Low ratios of lecithin t o protein in SAM are found before 135 days of gestation. Subsequently, the amount of lecithin increases and, although protein also increases, the ratio increases 4-fold (Fig. 8). The amount of lung required t o reduce surface tension of 1 cm2 t o 1 2 dynes tended to decrease with advancing gestational age ( Fig. 9 and Table 1). Parallel studies of airway generation demonstrate a similarity t o the human fetal lung. Thus, the structural, compositional, and physiologic changes described in our studies strongly support the use of the fetal monkey for studies of developmentally related disorders of the human lung. SpeculationBiochemical and functional maturational changes in the fetal M . nemestrina indicate its suitability for studies of developmentally related pulmonary disorders of the human. Premature delivery by cesarean section between 1 3 0 and 1 4 0 days should provide a satisfactory homolog for hyaline membrane disease.Body and lung growth in the primate M. nemestrina in the last third of gestation has been described in a previous paper (19). The biochemical and physiologic maturation of the lung in this primate from 107 days of gestation through term (168 days) is the subject of this report. Boyden (3) has shown that develop ment of the terminal air sacs and airways in M. nemestrinn closely resembles that of the human. Maturational events in the primate M. nernestrina are presented, demonstrating the suitability of this primate for studies of human fetal lung development and clinically associated abnormalities. MATERIALS AND METHODSThe lungs of 23 fetal and 2 newborn M. gemestrina were obtained as previously described (19). In most cases, either the 1 right upper lobe or the medial basal (rose) lobule was removed for microscopic studies. Static pressure volume curves were obtained from the remaining lung. Deflation volumes after the second inflation were recorded at intervals between 35 and 0 cm H 2 0 transpulmonary pressure (4). Weights of the individual lobes were then obtained and samples were taken for determin...
To determine whether the cause of reduced total lung capacity (TLC) in hyaline membrane disease (HMD) is due to alveolar collapse, alveolar edema, or both, TLC was measured by N2-washout in premature Macaca nemestrina monkeys during the first 3 h of life. The TLC of animals with HMD was only one-third that of healthy premature monkeys over the first 3 h of life (p less than 0.01). At 3.5 h, lung tissue was rapidly frozen in situ during lung inflation to TLC. Samples of frozen lung tissue were freeze dried, embedded, sectioned, and examined by point counting. Animals with HMD had alveolar saccules filled with the residue of proteinaceous fluid, but little alveolar collapse was noted. The proportion of points falling on empty alveolar spaces was 74% in the healthy animals but only 18% in animals with HMD (p less than 0.01); there was a 70-fold increase in the residue present in alveoli of animals with HMD (p less than 0.05). In a separate experiment, rapid serial measurements of TLC by N2-washout showed that healthy premature monkeys, but not those with HMD, have a steady increase in TLC during the first few minutes of life, presumably due to clearance of lung liquid. Although the initial cause of reduced TLC in HMD appears to be inadequate clearance of fetal lung liquid, by 3 h of age proteinaceous alveolar edema is primarily responsible.
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