Alveolar endotoxin increases alveolar liquid clearance in rats

Garat, Chrystelle; Rezaiguia, S.; Meignan, Michel; D'Ortho, M. P.; Harf, Alain; Matthay, Michael A.; Jayr, Christian

doi:10.1152/jappl.1995.79.6.2021

Cited by 48 publications

(42 citation statements)

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“…The authors, using a model of perfused LPS, excluded the presence of pulmonary oedema as a potential cause of protein increase in the BALF, since it could not be demonstrated even at ultrastructural level. Other authors did not observe changes in extravascular lung water after LPS tracheal instillation, by means of gravimetric determination of extravascular water and dry weight [35].…”

Section: Discussionmentioning

confidence: 87%

“…The protein obtained in the BALF could have been the result of local liberation of inflammatory mediators since no alveolar oedema was found in the histopathological analysis. Another explanation could be the stimulatory effect of alveolar endotoxin on alveolar fluid clearance as demonstrated by GARAT et al [35]. In a model of tracheally instilled LPS in rats, GARAT et al [35] observed no changed in extravascular lung water and lung permeability to protein, although a marked increase in inflammatory cells in the air spaces was detected.…”

Section: Discussionmentioning

confidence: 96%

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Respiratory effects of lipopolysaccharide-induced inflammatory lung injury in mice

Faffe¹,

Seidl²,

Chagas³

et al. 2000

eur respir j

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The pathogenic mechanisms of lipopolysaccharide (LPS)-induced lung injury have not been classified. This study examined the physiological changes after endotoxin inhalation and related those to features of pulmonary inflammation in mice.Pulmonary mechanics, histopathology, and bronchoalveolar lavage fluid (BALF) from BALB/c mice were analysed at different occasions (3, 24, 48 and 72 h) after inhalation of saline or LPS from Excherichia coli (0.3 (L0.3) or 10 mg . mL -1 (L10)). Mice were sedated, anaesthetized, and ventilated. After chest wall resection static (Est) and dynamic (Edyn) elastances, DE (Edyn-Est), resistive (DP1) and viscoelastic/ inhomogeneous pressures (DP2), and DP1+DP2 (DPtot) were obtained by end-inflation occlusion method. Lungs were prepared for histopathology. In parallel groups, tumour necrosis factor (TNF)-a, neutrophils, and protein were evaluated in the BALF.L0.3 and L10 showed a time-dependent production of TNF-a preceding a massive neutrophil infiltration. In L10 BALF there was an increase in protein level at 24 and 48 h. Est and Edyn increased early in L0.3 (65%, 63%) and L10 (41%, 51%). In L10 DE, DP2, and DPtot showed a gradual rise. At 72 h all groups were similar. L0.3 showed an early increase in cellularity, which returned to normal at 72 h. L10 presented the same pattern with the cell count remaining elevated until 72 h.In conclusion, lipopolysaccharide inhalation led to elastic and viscoelastic pulmonary changes together with tumour necrosis factor-a production and neutrophil infiltration in mouse lung. Eur Respir J 2000; 15: 85±91.

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Section: Discussionmentioning

confidence: 87%

Section: Discussionmentioning

confidence: 96%

Respiratory effects of lipopolysaccharide-induced inflammatory lung injury in mice

Faffe¹,

Seidl²,

Chagas³

et al. 2000

eur respir j

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“…The simplest explanation would be that of remodeling of the alveolar-capillary membranes, which occurs in CHF. 3,6 Note that epidermal growth factor upregulates alveolar epithelial sodium transport, 1 tumor necrosis factor-␣ mediates an upregulation of sodium and fluid transfer in a rat model, 20 and cardiac glycosides are potent inhibitors of alveolar fluid clearance. 21 …”

Section: Saline DL Co and Its Subdivisionsmentioning

confidence: 99%

Impeded Alveolar-Capillary Gas Transfer With Saline Infusion in Heart Failure

et al. 1999

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Abstract-The microvascular pulmonary endothelium barrier is critical in preventing interstitial fluid overflow and deterioration in gas diffusion. The role of endothelium in transporting small solutes in pathological conditions, such as congestive heart failure (CHF), has not been studied. Monitoring of pulmonary gas transfer during saline infusion in CHF was used to probe this issue. Carbon monoxide diffusion (DL CO ), its membrane diffusion (D M ) and capillary blood volume (V C ) subcomponents, and mean right atrial (rap) and mean pulmonary wedge (wpp) pressures after saline or 5% .01 versus 750 mL of saline) and decreased V C (Ϫ9, PϽ0.01 versus 750 mL of saline); aldosterone (Ϫ40%), renin (Ϫ41%), hematocrit (Ϫ3%), rap, and wpp behaved as they did after saline infusion. In controls, responses to both saline amounts were similar to responses in CHF patients regarding aldosterone, renin, hematocrit, rap, and wpp, whereas DL CO , D M , and V C values tended to rise. Hindrance to gas transfer (reduced DL CO and D M ) with salt infusion in CHF, despite an increase in V C and no variations in pulmonary hydrostatic forces, indicates an upregulation in sodium transport from blood to interstitium with interstitial edema. Redistribution of blood from the lungs, facilitating interstitial fluid reabsorption, or sodium uptake from the alveolar lumen by the sodium-glucose cotransport system might underlie the improved alveolar-capillary conductance with glucose. (Hypertension. 1999;34:1202-1207.)Key Words: capillaries Ⅲ epithelium Ⅲ glucose Ⅲ heart failure Ⅲ sodium F or the lung parenchyma to allow gas exchange between blood and gas in the alveoli, a continuous clearance is required of the excess of fluid into the interstitial space and the alveolar lumen. Excessive water accumulation in these compartments is called pulmonary and alveolar edema, respectively. The pulmonary microvascular endothelium and the alveolar epithelium constitute a barrier that is critical for gas exchange and modulation of fluid and solute passage between blood, the interstitial compartment, and alveoli. 1 Despite the substantial progress that has been made in understanding the physiology of the endothelial and epithelial layers in regulating lung fluid balance, further study regarding the local and systemic regulatory factors under pathological conditions is necessary. 1 An imbalance in hydrostatic forces is interpreted as the basic mechanism for volume overload and cardiogenic pulmonary edema. 2 In congestive heart failure (CHF), pulmonary edema may be absent despite elevation of the hydrostatic pressures 3 or may be present even if pressures are normal. 4 Whether altered hemodynamics are the exclusive mechanisms for pulmonary edema in CHF and whether alterations in the capillary endothelium and/or in the alveolar epithelium barrier contribute to changes in salt, water, and gas transfer have been the subjects of only limited research. 3 Cardiogenic anatomic injuries of the alveolar-capillary membrane have been reported in animals and humans. 5,6 ...

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“…This impairment is caused by increased mucus viscosity and adhesiveness due to the loss of water [37]. Endotoxin and bacteria were shown to increase fluid transport across the alveolar epithelium [38,39] in part by a TNF-a-dependent mechanism [39].…”

Section: Discussionmentioning

confidence: 99%

Fibronectin and α5ß1 integrin mediate binding of <I>Pseudomonas aeruginosa</I> to repairing airway epithelium

Roger¹,

Puchelle²,

Bajolet-Laudinat³

et al. 1999

Eur Respir J

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Adrenalectomy permits a late, local TNF-a release in LPS-challenged rat airways. A. Miller-Larsson, A. Runstro Èm, R. Brattsand. #ERS Journals Ltd 1999. ABSTRACT: The normal rise of circulating endogenous glucocorticosteroids (GCS), in response to immunological stimuli, can be impaired in patients with inflammatory diseases. The aim of this study was to investigate whether abolition of the endogenous GCS response promotes local production of the pro-inflammatory cytokine, tumour necrosis factor (TNF)-a, in challenged airways and affects the cellular response in rats.In adrenalectomized or sham operated rats, the trachea and main bronchi were lavaged at various times after intratracheal instillation of low dose lipopolysaccharide (LPS). TNF-a in lavage fluid and plasma corticosterone were measured, and cells were differentiated.In adrenalectomized rats, LPS-induced in the airways a biphasic TNF-a release peaking at 2 and 6 h, whereas in sham operated rats the second peak was absent; probably inhibited by the strong rise of plasma corticosterone. The second peak was abolished in adrenalectomized rats by pretreatment with exogenous GCS. The LPSinduced neutrophil influx and a decrease in mononuclear cells were prolonged in adrenalectomized rats.In conclusion, abolition of the endogenous glucocorticosteroid response promotes the late release of tumour necrosis factor-a in the airways and prolongs the cellular response. This suggests that a normal rise of endogenous glucocorticosteroid after an immunological trigger contributes to a dampening of the late inflammatory activity. Eur Respir J 1999; 13: 1310±1317.

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Alveolar endotoxin increases alveolar liquid clearance in rats

Cited by 48 publications

References 0 publications

Respiratory effects of lipopolysaccharide-induced inflammatory lung injury in mice

Respiratory effects of lipopolysaccharide-induced inflammatory lung injury in mice

Impeded Alveolar-Capillary Gas Transfer With Saline Infusion in Heart Failure

Fibronectin and α5ß1 integrin mediate binding of <I>Pseudomonas aeruginosa</I> to repairing airway epithelium

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