The Effects of Intravenous Infusion of Saline on Lung Density, Lung Volumes, Nitrogen Washout, Computed Tomographic Scans, and Chest Radiographs in Humans<sup>1–</sup><sup>3</sup>

Coates, G. Glenn; Powles, A. C. Peter; Morrison, Stuart C.; Sutton, J. R.; Webber, Colin E.; Zylak, Carl J.

doi:10.1164/arrd.1983.127.1.91

Cited by 16 publications

(4 citation statements)

References 16 publications

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“…A very mild restrictive pattern also occurred, as suggested by the decrease in FEV 1 and FVC. These data are in line with previous reports, where infusion of a similar amount of saline had similar effects in lung function [33], [34], [35], [36] and DLCO [6], [25], [37].…”

Section: Discussionsupporting

confidence: 93%

Role of Alveolar β2-Adrenergic Receptors on Lung Fluid Clearance and Exercise Ventilation in Healthy Humans

et al. 2013

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BackgroundIn experimental conditions alveolar fluid clearance is controlled by alveolar β2-adrenergic receptors. We hypothesized that if this occurs in humans, then non-selective β-blockers should reduce the membrane diffusing capacity (DM), an index of lung interstitial fluid homeostasis. Moreover, we wondered whether this effect is potentiated by saline solution infusion, an intervention expected to cause interstitial lung edema. Since fluid retention within the lungs might trigger excessive ventilation during exercise, we also hypothesized that after the β2-blockade ventilation increased in excess to CO2 output and this was further enhanced by interstitial edema.Methods and Results22 healthy males took part in the study. On day 1, spirometry, lung diffusion for carbon monoxide (DLCO) including its subcomponents DM and capillary volume (VCap), and cardiopulmonary exercise test were performed. On day 2, these tests were repeated after rapid 25 ml/kg saline infusion. Then, in random order 11 subjects were assigned to oral treatment with Carvedilol (CARV) and 11 to Bisoprolol (BISOPR). When heart rate fell at least by 10 beats·min−1, the tests were repeated before (day 3) and after saline infusion (day 4). CARV but not BISOPR, decreased DM (−13±7%, p = 0.001) and increased VCap (+20±22%, p = 0.016) and VE/VCO2 slope (+12±8%, p<0.01). These changes further increased after saline: −18±13% for DM (p<0.01), +44±28% for VCap (p<0.001), and +20±10% for VE/VCO2 slope (p<0.001).ConclusionsThese findings support the hypothesis that in humans in vivo the β2-alveolar receptors contribute to control alveolar fluid clearance and that interstitial lung fluid may trigger exercise hyperventilation.

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Section: Discussionsupporting

confidence: 93%

Role of Alveolar β2-Adrenergic Receptors on Lung Fluid Clearance and Exercise Ventilation in Healthy Humans

et al. 2013

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“…Rapid intravenous infusion of an isosmotic solution, such as saline 0.9%, is expected to be followed by fluid leakage from both pulmonary and bronchial vessels (7,10,13,16,22,(30)(31)(32)(33). The ensuing events include filling of the spaces around the alveoli and the complex vascular network accompanying the airways (29), likely promoted by negative interstitial pressure.…”

Section: Discussionmentioning

confidence: 99%

“…Experimental evidence in animals demonstrates that airway wall edema resulting from vascular engorgement increases peripheral airway resistance (13,30) and potentiates the response to chemical constrictor agents (4,30). In humans, the few studies in which rapid intravenous saline infusion was used with the intent to render the airway wall edematous and thick have documented mild airflow obstruction (10), air trapping (7,22), and a leftward shift of the doseresponse curve to methacholine (27). No systematic changes in elastic recoil of the lung were reported (22).…”

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confidence: 99%

Effects of rapid saline infusion on lung mechanics and airway responsiveness in humans

Pellegrino¹,

Dellacà²,

Macklem³

et al. 2003

Journal of Applied Physiology

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. Effects of rapid saline infusion on lung mechanics and airway responsiveness in humans. J Appl Physiol 95: 728-734, 2003. First published May 2, 2003 10.1152/japplphysiol.00310.2003.-Lung mechanics and airway responsiveness to methacholine (MCh) were studied in seven volunteers before and after a 20-min intravenous infusion of saline. Data were compared with those of a time point-matched control study. The following parameters were measured: 1-s forced expiratory volume, forced vital capacity, flows at 40% of control forced vital capacity on maximal (V m40) and partial (V p40) forced expiratory maneuvers, lung volumes, lung elastic recoil, lung resistance (RL), dynamic elastance (Edyn), and within-breath resistance of respiratory system (Rrs). RL and Edyn were measured during tidal breathing before and for 2 min after a deep inhalation and also at different lung volumes above and below functional residual capacity. Rrs was measured at functional residual capacity and at total lung capacity. Before MCh, saline infusion caused significant decrements of forced expiratory volume in 1 s, V m40, and V p40, but insignificantly affected lung volumes, elastic recoil, RL, Edyn, and Rrs at any lung volume. Furthermore, saline infusion was associated with an increased response to MCh, which was not associated with significant changes in the ratio of V m40 to V p40. In conclusion, mild airflow obstruction and enhanced airway responsiveness were observed after saline, but this was not apparently due to altered elastic properties of the lung or inability of the airways to dilate with deep inhalation. It is speculated that it was likely the result of airway wall edema encroaching on the bronchial lumen.

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“…4,11 These same changes are seen in early pulmonary edema. 5 There is other indirect evidence for a small increase in lung water on acute exposure to altitude. We have reported, in four volunteers using a Compton scatter technique, an increased lung mass after 10 hours at 446 Torr in a hypobaric chamber.…”

Section: Sub-clinical Pulmonary Edemamentioning

confidence: 99%

High-Altitude Pulmonary Edema

Coates¹

1981

Semin Respir Crit Care Med

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Early clinical descriptions of high altitude pulmonary edema (HAPE) are to be found in the works of Ravenhill, Hurtado, Houston, and Stewart. 16,21,33,38 However, the earliest reported case may be that of a physician climber on Mt. Blanc in 1891, described by Mosso. 26 For those readers interested in a comprehensive and practical review of HAPE, the recent reviews by Hultgren are recommended. 17,20 The purpose of this article is to review possible mechanisms responsible for HAPE and to present preliminary data obtained from the sheep chronic lymph fistulae model subjected to hypobaric hypoxia.There is no single unifying hypothesis that has explained the clinical, laboratory, and pathologic findings in patients with HAPE, but several mechanisms have been proposed. The most obvious hypothesis is that hypoxia itself causes damage to pulmonary capillaries. DIRECT EFFECT OF HYPOXIA ON PULMONARY CAPILLARY PERMEABILITYAlthough there is evidence that total anoxia 15 and ischemia 7 cause increased permeability of systemic capillaries there is no evidence that hypoxia affects pulmonary capillary permeability. Staub has already discussed the chronically instrumented sheep model that is used to detect changes in fluid and protein flux in the lungs. Using this model, Bland and associates showed that in adult sheep breathing 10 percent O 2 for 48 hours there was no change in pulmonary microvascular filtration of fluid or permeability to plasma proteins. 1 Other experiments support the view that, by itself, even profound hypoxia does not cause pulmonary edema in adult animals. 28,44 On the other hand Bressack and Bland have shown an increased lung fluid filtration in newborn lambs breathing 10 percent O 2 for 6 hours. 2 This may be relevant to HAPE since there is a much higher incidence of HAPE in children than in adults. 34 It is possible that hypobaria in addition to hypoxia will cause changes in lung lymph flow. To examine this possibility we have determined the effect of hypobaric hypoxia on lymph flow and lymph protein concentration in sheep. The preliminary data indicate that decompression to 380 Torr (18,000 ft) for 24 hours has no effect on lymph flow or lymph protein concentration ( Fig. 1). Figure 1. The effect of hypobaric hypoxia on lung lymph flow, lymph protein concentration pulmonary artery and left atrial pressure in a sheep. The only change is an increase in pulmonary artery pressure.

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The Effects of Intravenous Infusion of Saline on Lung Density, Lung Volumes, Nitrogen Washout, Computed Tomographic Scans, and Chest Radiographs in Humans^1–³

Cited by 16 publications

References 16 publications

Role of Alveolar β2-Adrenergic Receptors on Lung Fluid Clearance and Exercise Ventilation in Healthy Humans

Role of Alveolar β2-Adrenergic Receptors on Lung Fluid Clearance and Exercise Ventilation in Healthy Humans

Effects of rapid saline infusion on lung mechanics and airway responsiveness in humans

High-Altitude Pulmonary Edema

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The Effects of Intravenous Infusion of Saline on Lung Density, Lung Volumes, Nitrogen Washout, Computed Tomographic Scans, and Chest Radiographs in Humans1–3

Cited by 16 publications

References 16 publications

Role of Alveolar β2-Adrenergic Receptors on Lung Fluid Clearance and Exercise Ventilation in Healthy Humans

Role of Alveolar β2-Adrenergic Receptors on Lung Fluid Clearance and Exercise Ventilation in Healthy Humans

Effects of rapid saline infusion on lung mechanics and airway responsiveness in humans

High-Altitude Pulmonary Edema

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The Effects of Intravenous Infusion of Saline on Lung Density, Lung Volumes, Nitrogen Washout, Computed Tomographic Scans, and Chest Radiographs in Humans^1–³