Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0034063 (pulmonary edema)
 10,665 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The causes of respiratory distress in O2 toxicity are not well understood. The purpose of this study was to better define the airway abnormalities caused by breathing 100% O2. Sheep were instrumented for measurements of dynamic compliance (Cdyn), functional residual capacity by body plethysmography (FRC), hemodynamics, and lung lymph flow. Each day Cdyn and FRC were measured before, during, and after the application of 45 min continuous positive airway pressure (CPAP) at 15 cmH2O. The amount of aerosol histamine necessary to reduce Cdyn 35% from baseline (ED35) was measured each day as was the response to aerosol metaproterenol. Cdyn decreased progressively from 0.083 +/- 0.005 (SE) 1/cmH2O at baseline to 0.032 +/- 0.004 l/cm H2O at 96 h of O2. Surprisingly, FRC did not decrease (1,397 +/- 153 ml at baseline vs. 1,523 +/- 139 ml at 96 h). The ED35 to histamine did not vary among days or from air controls. Metaproterenol produced a variable inconsistent increase in Cdyn. We also measured changes in Cdyn during changes in respiratory rate and static pressure-volume relationships in five other sheep. We found a small but significant frequency dependence of compliance and an increase in lung stiffness with O2 toxicity. We conclude that in adult sheep O2 toxicity reduces Cdyn but does not increase airway reactivity. The large reduction in Cdyn in O2 toxicity results from processes other than increased airway reactivity or reduced lung volume, and Cdyn decreases before the development of lung edema.
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PMID:Lung mechanics and airway reactivity in sheep during development of oxygen toxicity. 227 71

The acute respiratory distress syndrome (ARDS) is a disorder of diffuse lung injury secondary to a wide variety of clinical insults (eg, sepsis) and is manifested by impaired oxygenation, pulmonary edema, and decreased static and dynamic compliance. More recently, airflow resistance has been shown to be increased in humans with ARDS. We designed a prospective, randomized, placebo-controlled, crossover trial to determine the presence and reversibility of increased airflow resistance in ARDS. We studied eight mechanically ventilated patients with ARDS (criteria: PaO2 < or = 70 mm Hg with FIO2 < or = 0.4; diffuse bilateral infiltrates; and pulmonary artery wedge pressure < or = 18 mm Hg). Each was intubated with a No. 8.0 orotracheal tube. We measured dynamic compliance (Cdyn), static compliance (Cstat), airflow resistance across the lungs (RL), shunt fraction (Qs/Qt on FIO2 = 1.0), minute ventilation (VE), PaO2/PAO2, and dead space to tidal volume ratio (VD/VT). Patients were blindly assigned to receive either metaproterenol (1 mL 0.5% in 3 mL saline solution) or saline solution (4 mL) aerosolized over 15 min 6 h apart and in random order so that patients served as their own controls. Metaproterenol significantly reduced RL, peak and plateau airway pressure, and increased Cdyn. Metaproterenol tended to increase PaO2/PAO2, but had no effect on pulmonary shunt or dead space ventilation. We conclude that the increase in airflow resistance of ARDS is substantially reversed by aerosolized metaproterenol without affecting dead space. These data suggest that abnormalities of RL are at lest partially due to bronchospasm.
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PMID:Effect of bronchodilators on lung mechanics in the acute respiratory distress syndrome (ARDS). 795 13