PubMed · 5361966
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G H Broeders. 1969. [Experiences with amnioscopy].. https://pubmed.ncbi.nlm.nih.gov/5361966/
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1. Most of the liquid that fills the lung of the fetal sheep in late gestation is cleared by the end of labour. Clearance of this liquid has a beneficial effect on postnatal gas exchange and therefore represents an important adaptation for postnatal life. Despite its importance, there is disagreement about whether clearance begins prior to labour, or occurs entirely within labour. 2. To address this issue, we made serial determinations of lung liquid volume by indicator dilution during late gestation and labour in the fetal sheep. 3. Regression analysis demonstrated that lung liquid volume exhibited a plateau level in the near-term fetus before it began to decline. Two models provided a fit to the decline in volume. In one, lung liquid clearance occurred in two linear phases, the first beginning 70 h before the study was terminated when the ewe was in advanced labour, the second occupying the last 8 h of the study period. In the initial phase, average lung liquid volume fell from 38.3 to 26.4 ml x kg(-1) before a rapid decline in the second phase reduced the volume to 13.8 ml x kg(-1). An exponential decay model was also found to fit the data; this showed a gradual decline in lung liquid volume in the 2 days preceding onset of labour, followed by a much more rapid decline within labour. 4. The rate of lung liquid secretion also declined in two linear phases, both of which commenced earlier than the changes in lung liquid volume. An exponential decay model also gave a significant fit to the data, but the fit was significantly weaker than that achieved with the two-slope model. 5. We conclude that clearance of lung liquid begins well before commencement of labour in the full term fetal sheep, and then accelerates once labour is established. In our study, lung liquid volume fell even in the absence of reabsorption of liquid across the pulmonary epithelium, indicating that outflow of liquid through the trachea must have occurred at a rate in excess of the secretion rate.
Epidemiological studies have shown that offspring of women who smoke during pregnancy have abnormal lung function and associated higher incidences of lower respiratory disorders. The recent identification of nicotinic acetylcholine receptors (nAChR) in fetal lung suggests that the direct interaction between nicotine and nAChR in fetal lung may underlie the postnatal pulmonary abnormalities seen in such infants. This hypothesis was tested in monkeys to determine if maternal nicotine exposure would produce changes in lung mechanics in newborn monkeys similar to those observed in human infants whose mothers smoked during pregnancy. Timed pregnant rhesus monkeys were infused with either nicotine (1.5 mg/kg/d, n = 7) or saline (n = 7) using subcutaneous osmotic pumps from Day 26 to 160 of gestation. On Day 160 of pregnancy (term = 165 d), fetuses were delivered by C-section, and the following day were subjected to pulmonary function testing. After testing, animals were sacrificed, and lungs weighed and fixed. Lung weight and fixed lung volume decreased (16% and 14%, respectively) significantly following in utero nicotine exposure. Peak tidal expiratory flow, FEV(0.2), mean mid-expiratory flow, forced expiratory volume at peak expiratory flow (FEV(PEF)), and FEV(PEF)/FVC% were significantly lower in newborns exposed to nicotine during gestation. Absolute and specific pulmonary resistance increased significantly whereas absolute and specific dynamic compliance remained unchanged in prenatally nicotine-treated pups. These changes in pulmonary function are strikingly similar to the changes observed in offspring of human smokers. This suggests that the interaction of nicotine with nAChR in developing lung is responsible for the altered pulmonary mechanics observed in human infants whose mothers smoked during pregnancy.
Intraamniotic endotoxin causes chorioamnionitis, which is followed by improved fetal lung function after 4 d in fetal sheep. We evaluated 0.1 mg, 1 mg, 4 mg, and 10 mg endotoxin for inflammation and lung maturation effects after 7 d. Four and 10 mg endotoxin caused similar lung maturation and inflammation in the lung and chorioamnion. The number of neutrophils in cord blood and the inflammatory cells in alveolar lavage and fetal lung tissue increased in a dose-dependent manner. Lower endotoxin doses induced indicators of chorioamnionitis, lung and systemic inflammation without inducing lung maturation. Therefore, some degree of inflammation can occur without subsequent lung maturation. The inflammatory changes caused by 4 mg endotoxin were assessed after 5 h, 24 h, 72 h, and 7 d to discern local versus systemic inflammation after intraamniotic endotoxin. At 5 h active inflammatory cells were in the airways producing hydrogen peroxide, and interleukin-6 and -8 were increased in the cord blood indicating both lung and systemic responses. Cells recruited into the amniotic fluid produced proinflammatory cytokine mRNA for 7 d with no cytokine mRNA in chorioamnion, lung, or spleen after 72 h. The cells in the amniotic fluid may be a source of prolonged fetal exposure to proinflammatory cytokines.