PubMed · 10325821
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B A Hills, I B Masters. 1999. 'Dewatering' the lungs.. https://doi.org/10.1136/fn.80.1.f78
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Chronic heart failure (CHF) disturbs the alveolar-capillary interface and increases the resistance to gas transfer. Alveolar-capillary membrane conductance (D(M)) and capillary blood volume (V(c)) are subcomponents of the lung diffusion capacity. Elevation of the capillary pressure causes alveolar-capillary membrane stress failure (i.e. increase in capillary permeability to water and ions, and disruption of local regulatory mechanisms for gas exchange), leading to a decrease in D(M), an increase in V(c) and subsequent impairment of diffusion capacity. Renewed recent interest in abnormalities in lung diffusion in patients with CHF has brought about new pathophysiological insights. A significant contribution of the altered gas transfer to the pathogenesis of exercise limitation and ventilatory abnormalities has been reported, and D(M) has been identified as the best lung function predictor of oxygen uptake at peak exercise. This review examines the pathophysiological and clinical significance of assessing lung diffusion capacity in patients with CHF.
The present article reviews the basic principles of a new approach to the characterization of pulmonary disease. This approach is based on the unique nuclear magnetic resonance (NMR) properties of the lung and combines experimental measurements (using specially developed NMR techniques) with theoretical simulations. The NMR signal from inflated lungs decays very rapidly compared with the signal from completely collapsed (airless) lungs. This phenomenon is due to the presence of internal magnetic field inhomogeneity produced by the alveolar air-tissue interface (because air and water have different magnetic susceptibilities). The air-tissue interface effects can be detected and quantified by magnetic resonance imaging (MRI) techniques using temporally symmetric and asymmetric spin-echo sequences. Theoretical models developed to explain the internal (tissue-induced) magnetic field inhomogeneity in aerated lungs predict the NMR lung behavior as a function of various technical and physiological factors (e.g., the level of lung inflation) and simulate the effects of various lung disorders (in particular, pulmonary edema) on this behavior. Good agreement has been observed between the predictions obtained from the mathematical models and the results of experimental NMR measurements in normal and diseased lungs. Our theoretical and experimental data have important pathophysiological and clinical implications, especially with respect to the characterization of acute lung disease (e.g., pulmonary edema) and the management of critically ill patients.
UNLABELLED: A soluble form of thrombomodulin (TM), an anticoagulant proteoglycan of the endothelial cell membrane, considered a marker of vascular endothelial damage, was measured in plasma of preterm infants with respiratory distress syndrome (RDS). In these patients, lung immaturity leads to endothelial leak of plasma proteins and to surfactant inhibition. In 18 babies with RDS, plasma TM concentration was significantly elevated compared with values of a matched group of babies without pulmonary disease (276.1 ng/ml vs 141.3 ng/ml) (P < 0.05). Furthermore, TM levels of mechanical ventilated babies (IPPV) with severe RDS were higher than those of babies with moderate RDS and treated with nasal CPAP (340.9 ng/ml vs 174.2 ng/ml) (P < 0.05). CONCLUSION: These data show that TM can be used as marker of pulmonary endothelial damage in preterm babies treated with mechanical ventilation for RDS and suggest early intervention with exogenous surfactant to limit alveolar protein leakage and surfactant inactivation.