Publications by authors named "Tierney D"

Many causes for the adult respiratory distress syndrome (ARDS) have been reported, all with common pathologic, pathophysiologic and biochemical end results. The final common pathway may involve changes in lung content of a critical enzyme, superoxide dismutase, or alterations in surfactant metabolism, or both. The early assumption that the disorder is partially due to oxygen toxicity from inspired oxygen concentrations greater than 60 percent is consistent with findings of recent biochemical studies.

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We compared several sets of conditions used to estimate metabolism in rat lung slices. 14CO2 production from [14C]glucose, oxygen consumption, lactate production, and glucose consumption were used as measures of metabolic activity. The calculated results differed when we used 1) different techniques for estimating tissue weight, 2) tissue slices of 0.

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Twenty pregnant rabbits were studied in pairs. Half were given cortisol subcutaneously on days 24, 25, and 26 of gestation in dosage of 2 mg/kg/day. Half served as controls and received saline.

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Air embolism with positive-pressure ventilation of rats.

J Appl Physiol Respir Environ Exerc Physiol

March 1977

Although air embolism is known to occur in humans and animals when the lung is overdistended, very few cases have been reported to be associated with positive-pressure ventilation. We have observed that air embolism occurs in rats ventilated with high inspiratory pressures (70 cmH2O) associated with high end-expiratory pressures (10 cmH2O). However, it does not occur in normal rats if the end-expiratory pressure is less than 5 cmH2O or the peak inspiratory pressure is below 60 cmH2O when the frequency of ventilation is 30.

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Pathogen-free rats were given either hydrocortisone (4 mg) or saline by intraperitoneal injection twice daily for 7 consecutive days. Lung weight, body weight, DNA, and total phosphatidylcholine content in lungs were equal in the saline and hydrocortisone groups. Lungs of rats receiving hydrocortisone had 23% more saturated phosphatidylcholine (P less than 0.

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Lung metabolism has been extremely difficult to determine in vivo primarily because the lung is overwhelmed by a great blood flow that generally makes the Fick principle inadequate. Largely for reasons such as this, investigators have had to rely on in vitro preparations. The isolated perfused lung has the apparent advantage of being similar to the lung in vivo when compared with other preparations.

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Using conventional concepts, it is possible that a single pathologic entity, pulmonary telangiectases, can produce hypoxia by 3 physiologic mechanisms; shunt, diffusion defect, and ventilation-perfusion abnormalities. The estimation of shunt or shunt-like effect is traditionally calculated by measuring the Po2 of arterial blood during the breathing of 100 per cent 02. This method, however, did not determine blood flow through large alveolar vessels in a patient with familial hemorrhagic telangiectasis who was severely hypoxemic while breathing air.

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To learn whether surface force changes precede the appearance of lung edema during experimental intoxication due to paraquat, we studied rats for 1 day following injection of 27 mg/kg iv. By 24 h, surface-active material recovered by lung lavage was decreased 32 percent, and changes in lung microsections and recoil pressure at half-deflation suggested decreased alveolar stability. Despite a 25 percent loss in overall body weight, lung weight increased more than 7 percent and protein concentration in lung lavage fluid increased by 158 percent.

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