Effect of lung inflation in vivo on airways  with smooth muscle tone or edema

Brown, Robert H.; Mitzner, Wayne; Bulut, Yasemin; Wagner, Elizabeth M.

doi:10.1152/jappl.1997.82.2.491

Cited by 40 publications

(34 citation statements)

References 23 publications

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“…Interestingly, the minimum values achieved at TLC were slightly, although significantly, higher than before MCh. All of these data are in line with two studies conducted in sheep, in which bronchial edema caused by bradykinin, an inflammatory mediator, did not prevent a full lung inflation from reversing MCh-induced airway narrowing (1,2). Thus it emerges that airway edema itself appears not to affect the ability of DI to reverse airflow obstruction.…”

Section: Discussionsupporting

confidence: 87%

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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Section: Discussionsupporting

confidence: 87%

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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“…They found that a 50% increase in airway wall oedema caused a 13% decrease in airway luminal area; and at high lung volume, luminal area was not affected by the oedema. These observations are consistent with another study in which the effects of lung volume on oedematous airways were measured using HRCT [158]. In that study, airway narrowing caused by wall oedema at low lung volume was completely reversed by lung expansion.…”

Section: Ahr and Lung Volumesupporting

confidence: 91%

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

An¹,

Bai²,

Bates³

et al. 2007

European Respiratory Journal

342

298

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Excessive airway obstruction is the cause of symptoms and abnormal lung function in asthma.As airway smooth muscle (ASM) is the effecter controlling airway calibre, it is suspected that dysfunction of ASM contributes to the pathophysiology of asthma. However, the precise role of ASM in the series of events leading to asthmatic symptoms is not clear. It is not certain whether, in asthma, there is a change in the intrinsic properties of ASM, a change in the structure and mechanical properties of the noncontractile components of the airway wall, or a change in the interdependence of the airway wall with the surrounding lung parenchyma. All these potential changes could result from acute or chronic airway inflammation and associated tissue repair and remodelling.Anti-inflammatory therapy, however, does not ''cure'' asthma, and airway hyperresponsiveness can persist in asthmatics, even in the absence of airway inflammation. This is perhaps because the therapy does not directly address a fundamental abnormality of asthma, that of exaggerated airway narrowing due to excessive shortening of ASM.In the present study, a central role for airway smooth muscle in the pathogenesis of airway hyperresponsiveness in asthma is explored.

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“…This result strongly suggests that vascular distention alone does not produce an increase in airway wall thickening. Airway wall thickening and edema formation have also been noted in sheep given bradykinin infusions into the bronchial circulation (24,25), as well as in isolated dog lungs made grossly edematous by saline infusions into a sealed pulmonary vasculature (26). Taken together, we believe that our findings coupled with these considerations strongly predict that membrane water permeability was reduced in the AQP1-null group.…”

Section: )supporting

confidence: 78%

Decreased pulmonary vascular permeability in aquaporin-1-null humans

King¹,

Nielsen²,

Agre³

et al. 2002

Proc. Natl. Acad. Sci. U.S.A.

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116

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The molecular determinants of water permeability in the human lung are incompletely defined. Aquaporins (AQP) are water-specific membrane channel proteins. AQP1 is present in endothelial cells in the lung, including those in the vascular plexus around the airways. Rare individuals have been identified who are deficient in AQP1. High-resolution computed tomography scans of the lung were used to evaluate the response to i.v. fluid challenge in two unrelated AQP1-null individuals and five normal controls. The airways and pulmonary vessels were measured at baseline and after i.v. administration of 3 liters of saline. Increases in airway wall thickness after fluid administration reflect peribronchiolar edema formation. Both control and AQP1 null subjects had approximately a 20% increase in pulmonary vessel area in response to saline infusion, suggesting similar degrees of volume loading. Control subjects had a 44% increase in the thickness of the airway wall, consistent with peribronchiolar edema formation. In marked contrast, airway wall thickness did not change in AQP1-null subjects in response to saline infusion. These studies indicate that AQP1 is a determinant of vascular permeability in the lung, and demonstrate a role for aquaporins in human pulmonary physiology. R egulation of water movement between the vascular, interstitial, and airway compartments is critical for normal lung function. Disruption of this process contributes to alterations in gas exchange, lung mechanics, and local lung defense mechanisms. However, the molecular determinants of water transport in the respiratory tract remain incompletely defined, particularly for human pathophysiology.Aquaporin-1 (AQP1), the archetypal membrane water channel protein, was initially described in red blood cells and renal proximal tubule epithelium (1). An extracellular epitope of AQP1 defines the Colton blood group antigen on red blood cells (2). Screening for anti-Colton antibodies by the International Blood Group Reference Laboratory identified only six Coltonnull kindreds worldwide; a seventh individual has recently been described (3). Individuals in three of these kindreds were evaluated, and each was found to be homozygous for a different mutation in the AQP1 gene with complete absence or marked reduction of AQP1 in red blood cell membranes (4). These individuals are unable to receive blood transfusions from normal donors, but otherwise reported no clinical symptoms as a consequence of AQP1 deficiency. Recent investigation of two AQP1-null individuals, however, revealed a decreased ability to concentrate urine maximally (5).AQP1 is abundantly expressed in pulmonary vascular endothelium, particularly in endothelial cells of the vascular plexus around the airways (6). This distribution suggests a role for AQP1 in regulation of vascular water permeability in the lung. In the present study, we provide the first functional assessment of any aquaporin in human lung. By using high-resolution computed tomography (HRCT) to examine the response to fluid challenge, ...

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Effect of lung inflation in vivo on airways with smooth muscle tone or edema

Cited by 40 publications

References 23 publications

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

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

Airway smooth muscle dynamics: a common pathway of airway obstruction in asthma

Decreased pulmonary vascular permeability in aquaporin-1-null humans

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