Alpha receptor influence on lung surfactant.
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Biomedical subjects
D R Bergren
Publications and source records attributed to D R Bergren.
Pulmonary surface tension and head injury.
Previous studies have shown that exposure of monkeys to lethal experimental head injury by means of a captive-bolt mechanism results in a decreased lung compliance and a high minimum surface tension. Such changes which occurred in the absence of any increase in lung weight/body weight ratios were ameliorated by the prior administration of various sympathetic blocking agents. Exposure of monkeys and cats to stimulation of the pulmonary sympathetics via the stellate ganglion also resulted in similar compliance and surface tension changes without any increase in lung weight. The present experiments were carried out in order to determine the effect of lethal mechanical head injury in the cat on the surface tension of the alveolar lining layer and reasons for any possible changes. Previous reports have shown that the addition of very small amounts of cholesterol to lung wash fluid raised the minimum surface tension to abnormal levels. The results from the present study show that a sudden lethal blow to the occiput in cats results in an abnormally high minimum surface tension (over 20 dynes/cm) in the lung wash fluid and a nearly 200% increase in cholesterol content. There was little or no change in lung wet weight/dry weight ratios or gross lung appearance following this head injury. Thus the results from the present study strongly suggests that the previously reported decreased lung compliance and high minimum surface tension following a blow to the head may be due in part at least to the presence of increased intra-alveolar cholesterol.
Animals↗
Hyperbaric oxygen and pulmonary surface tension.
Previous work has shown that short-term exposure of cats to oxygen at high pressure (OHP), to the extent of overt convulsive seizures, has little or no effect on the lung appearance or lung weight but does alter the alveolar surfactants. More prolonged exposure results in hemorrhagic edema of the cat lung similar to that observed in rats after only short-term exposure. Previous work showed that sympathetic stimulation via the stellate ganglion and mechanical CNS injury results in altered surfactants attributed to increased intra-alveolar cholesterol. In the present study, cats exposed to OHP until the animals convulsed intermittently for 3 min (approximately 1 hour, 6 ATA) similarly showed altered surfactants with a high minimum surface tension and a 150% increase in intra-alveolar cholesterol. These changes also occurred in the absence of any gross lung injury. The results from the present study suggest that an important causal mechanism involved in the development of gross lung injury associated with prolonged OHP exposure is an initial increase in minimum surface tension due to increased intra-alveolar cholesterol.
Animals↗