Effect of edema and height on bronchial diameter and shape in excised dog lung

Lai-Fook, S. J.; Beck, Kenneth C.; Sutcliffe, Alison M.; Donaldson, Jonathan T.

doi:10.1016/0034-5687(84)90024-0

Cited by 22 publications

(7 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…4). A role for this mechanism is supported by studies in which extra-alveolar airways have reduced diameters because of pancreatitis-induced inflammatory changes in rats (28), in excised dog lungs with hydrostatic edema (29), and when peri-bronchial edema is induced in sheep (30). Peripheral airway resistance is also increased after an elevation in left atrial pressure and extra-alveolar edema (13–15).…”

Section: Resultsmentioning

confidence: 99%

Perivascular fluid cuffs decrease lung compliance by increasing tissue resistance*

Lowe

Alvarez

King

et al. 2010

Critical Care Medicine

View full text Add to dashboard Cite

Objective-Lung inflammation causes perivascular fluid cuffs to form around extra-alveolar blood vessels; however, the physiologic consequences of such cuffs remain poorly understood. Herein, we tested the hypothesis that perivascular fluid cuffs, without concomitant alveolar edema, are sufficient to decrease lung compliance.Design-Prospective, randomized, controlled study. Setting-Research laboratory. Subjects-One hundred twenty male CD40 rats.Interventions-To test this hypothesis, the plant alkaloid thapsigargin was used to activate store-operated calcium entry and increase cytosolic calcium in endothelium. Thapsigargin was infused into a central venous catheter of intact, sedated, and mechanically ventilated rats.Measurements-Static and dynamic lung mechanics and hemodynamics were measured continuously.Main Results-Thapsigargin produced perivascular fluid cuffs along extra-alveolar vessels but did not cause alveolar flooding or blood gas abnormalities. Lung compliance dose-dependently decreased after thapsigargin infusion, attributable to an increase in tissue resistance that was attributed to increased tissue damping and tissue elastance. Airway resistance was not changed. Neither central venous pressure nor left ventricular end diastolic pressure was altered by thapsigargin. Heart rate did not change, although thapsigargin decreased pressure over time sufficient to reduce cardiac output by 50%. Infusion of the type 4 phosphodiesterase inhibitor, rolipram, prevented thapsigargin from inducing perivascular cuffs and decreasing lung compliance. Rolipram also normalized pressure over time and corrected the deficit in cardiac output.Conclusions-Our findings resolve for the first time that perivascular cuff formation negatively impacts mechanical coupling between the bronchovascular bundle and the lung parenchyma, decreasing lung compliance without impacting central venous pressure. Keywordspermeability; endothelium; thapsigargin; store-operated calcium entry; acute respiratory distress syndromeThe authors have not disclosed any potential conflicts of interest. The pulmonary endothelium normally serves as a tightly regulated barrier between blood and interstitium. However, endothelial barrier function is compromised in the blood vessels of critically ill patients with acute lung injury or acute respiratory distress syndrome (ARDS). Endothelial cell barrier disruption causes fluid accumulation in the lung parenchyma, which ultimately leads to inefficient gas exchange and decreased alveolar ventilation, and also in perivascular spaces surrounding extra-alveolar arteries and veins (1). Traditional thinking advocates that capillary endothelial cell barrier disruption increases interstitial fluid accumulation that is pulled by negative interstitial pressure into perivascular spaces of larger vessels as a safety mechanism that limits alveolar flooding. However, recent acute lung injury and pulmonary edema animal models indicate that extra-alveolar vessels exhibit greater permeability responses than do capillarie...

show abstract

Section: Resultsmentioning

confidence: 99%

Perivascular fluid cuffs decrease lung compliance by increasing tissue resistance*

Lowe

Alvarez

King

et al. 2010

Critical Care Medicine

View full text Add to dashboard Cite

show abstract

“…The mechanism by which intrapulmonary airways and smooth muscle within their walls are stretched by inspiration is largely due to the increase in radial traction on the airways exerted by the surrounding lung parenchyma (21)(22)(23). Edema of the airway wall or in the peribronchial space could unlink the interdependence between the airway and parenchyma resulting in a decrease in radial force acting on the smooth muscle with DI (24,25). Ingram considered the interaction between the airways and lung parenchyma and proposed that the attenuated response to DI in asthma is due to a problem of increased parenchymal relative to airway hysteresis (26,27).…”

Section: Discussionmentioning

confidence: 99%

Airway hyperresponsiveness in asthma: a problem of limited smooth muscle relaxation with inspiration.

Skloot¹,

Permutt²,

Togias³

1995

J. Clin. Invest.

443

351

View full text Add to dashboard Cite

We hypothesized that hyperresponsiveness in asthma is caused by an impairment in the ability of inspiration to stretch airway smooth muscle. If the hypothesis was correct, we reasoned that the sensitivity to inhaled methacholine in normal and asthmatic subjects should be the same if the challenge was carried out under conditions where deep inspirations were prohibited. 10 asthmatic and 10 normal subjects received increasing concentrations of inhaled methacholine under conditions where forced expirations from a' normal end-tidal inspiration were performed. When no deep inspirations were allowed, the response to methacholine was similar in the normal and asthmatic subjects, compatible with the hypothesis we propose. Completely contrary to our expectations, however, was the marked responsivity to methacholine that remained in the normal subjects after deep breaths were initiated. 6 of the 10 normal subjects had > 20% reduction in forced expiratory volume in one second (FEV 1) at doses of methacholine < 8 mg/ml, whereas there was < 15% reduction with 75 mg/ml during routine challenge. The ability of normal subjects to develop asthmatic responses when the modulating effects of increases in lung volume was voluntarily suppressed suggests that an intrinsic impairment of the ability of inspiration to stretch airway smooth muscle is a major feature of asthma. (J. Clin. Invest. 1995Invest. . 96:2393Invest. -2403

show abstract

“…Under normal conditions, lung inflation causes the surrounding lung parenchyma to increase its radial traction on the intraparenchymal airways and to distend them (18,20). Inflammation and edema in the airway wall might thus be expected to attenuate the magnitude of this radial traction produced by lung inflation (16,17,19). However, recent work using direct visualization of airways has failed to demonstrate any decrease in the outer border of the airway during acute airway edema (6).…”

mentioning

confidence: 99%

“…This would be consistent with several observations showing that a deep inspiration does not relieve bronchoconstriction in asthmatic patients (2, 3, 11-13, 23, 24). Several authors have proposed that, in asthma, edema fluid from inflammation and cellular infiltrate collects between the airway smooth muscle and the surrounding lung parenchyma and that this fluid should attenuate the forces of radial traction produced by increased lung volume (16,17,19). Our present findings in the sheep do not support this mechanism.…”

mentioning

confidence: 99%

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

Brown¹,

Mitzner

Bulut³

et al. 1997

Journal of Applied Physiology

View full text Add to dashboard Cite

Fibrous attachments to the airway wall and a subpleural surrounding pressure can create an external load against which airway smooth muscle must contract. A decrease in this load has been proposed as a possible cause of increased airway narrowing in asthmatic individuals. To study the interaction between the airways and the surrounding lung parenchyma, we investigated the effect of lung inflation on relaxed airways, airways contracted with methacholine, and airways made edematous by infusion of bradykinin into the bronchial artery. Measurements were made in anesthetized sheep by using high-resolution computed tomography to visualize changes in individual airways. During methacholine infusion, airway area was decreased but increased minimally with increases in transpulmonary pressure. Bradykinin infusion caused a 50% increase in airway wall area and an small decrease in airway luminal area. In contrast to airways contracted with methacholine, the luminal area after bradykinin increased substantially with increases in transpulmonary pressure, reaching 99% of the relaxed area at total lung capacity. Thus airway edema by itself did not prevent full distension of the airway at lung volumes approaching total lung capacity. Therefore, we speculate that if a deep inspiration fails to relieve airway narrowing in vivo, this must be a manifestation of airway smooth muscle contraction and not airway wall edema.

show abstract

Effect of edema and height on bronchial diameter and shape in excised dog lung

Cited by 22 publications

References 11 publications

Perivascular fluid cuffs decrease lung compliance by increasing tissue resistance*

Perivascular fluid cuffs decrease lung compliance by increasing tissue resistance*

Airway hyperresponsiveness in asthma: a problem of limited smooth muscle relaxation with inspiration.

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

Contact Info

Product

Resources

About