Evaluation of two-way protein fluxes across the alveolo-capillary membrane by scintigraphy in rats: effect of lung inflation

Prost, Nicolas de; Dreyfuss, Didier; Saumon, Georges

doi:10.1152/japplphysiol.00742.2006

Cited by 31 publications

(20 citation statements)

References 52 publications

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“…This result suggests that the contribution of mechanisms other than lung strain to the development of VILI, such as those occurring at low lung volume, is relatively more important. The lung strain threshold reported by these authors is consistent with the existence of an airway pressure threshold above which dramatic increases in lung microvascular permeability occur [4,17]. When the lung strain applied was accounted for, the time to achieve VILI was greater in larger animals than in smaller ones, implying that the former are more resistant to VILI than the latter.…”

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confidence: 70%

Modeling the time-course of ventilator-induced lung injury: what can we learn from interspecies discrepancies?

2011

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Alterations in lung fluid balance, increases in endothelial and epithelial permeability, and severe tissue damage have been widely described in animals following injurious mechanical ventilation and regrouped under the term ventilator-induced lung injury (VILI) [1]. The clinical relevance of VILI was highlighted by the acute respiratory distress syndrome (ARDS) Network trial that showed a 22% reduction of mortality in patients with ARDS when the mechanical stress applied to the lungs was lessened by reducing the tidal volume applied [2]. The pathophysiology of VILI is unequivocal, and several mechanical determinants of VILI have been identified to date: (1) regional overdistension caused by the application of a local stress or pressure that forces cells and tissues to assume shapes and dimensions that they do not assume during unassisted breathing [3][4][5]; (2) so-called ''low volume injury'' associated with the cyclic recruitment-derecruitment of lung units [6], which causes abrasion of the epithelial airspace lining by interfacial forces [7]; (3) inactivation of surfactant triggered by large alveolar surface area oscillations [8]; (4) the interdependence mechanism that raises cell and tissue stress between neighboring structures with differing mechanical properties [9]. Early experimental studies demonstrated that the main determinant of VILI is lung end-inspiratory volume, associated with high transpulmonary pressures [10,11]. Thus, the term ''volutrauma'' is preferred to the term ''barotrauma'', since the absolute level of airway pressure per se is not injurious [10].The severity of VILI depends both on the degree (as determined by ventilator settings) and duration of the mechanical insult applied to the lungs and on the sensitivity of the lungs to VILI, which differs according to animal species. For example, Webb and Tierney demonstrated that rats subjected to mechanical ventilation using peak inspiratory pressures of 30 or 45 cmH 2 O developed pulmonary edema within 60 and 20 min, respectively, following its onset [3], and Dreyfuss et al. showed that pulmonary edema occurred after only 5 min of injurious mechanical ventilation in healthy rats [5]. In contrast, in larger animal species, longer ventilation periods and higher peak inspiratory pressures are required for the development of VILI: lambs mechanically ventilated at 58 cmH 2 O peak inspiratory pressures for 6 h only developed mild pulmonary edema [12], and the average time required for the development of impairment in gas exchanges and pulmonary mechanics in sheep ventilated with 50 cmH 2 O peak inspiratory pressures was 24 h [13].

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confidence: 70%

Modeling the time-course of ventilator-induced lung injury: what can we learn from interspecies discrepancies?

2011

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“…Large inflationary pressures have been shown to increase epithelial barrier permeability [28,29]. An increase in epithelial barrier permeability after DI would favour greater airway narrowing in challenges preceded by DI.…”

Section: Discussionmentioning

confidence: 99%

The mechanism of deep inspiration-induced bronchoprotection: evidence from a mouse model

Wong¹,

Larcombe

Fernandes

et al. 2012

Eur Respir J

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In healthy individuals, deep inspirations (DIs) taken prior to a bronchial challenge reduce the bronchoconstrictor response, which is termed ''bronchoprotection''. The mechanism(s) of DI-induced bronchoprotection is unclear.The forced oscillation technique was used to assess the effect of prior DI on subsequent bronchoconstriction to methacholine (MCh) in BALB/c mice. We assessed likely mechanisms for the bronchoprotective effects of DI including reduced airway narrowing (from changes in airway resistance) and/or closure (changes in tissue elastance) and enhanced bronchodilation to a subsequent DI (% reversal in airway narrowing).DI prior to MCh challenge: 1) did not reduce but instead enhanced airway narrowing (p,0.05); 2) increased ventilation heterogeneity (p,0.05); 3) enhanced the subsequent bronchodilatory response to DI (p,0.05); and 4) reduced tissue elastance (p,0.05), suggesting opening of closed airways or alveoli units.Our findings suggest that DI prior to MCh challenge may elicit a series of changes, some of which are beneficial to respiratory function (enhanced bronchodilation), while others place greater load on the system (enhanced bronchoconstriction and ventilation heterogeneity). It is proposed that the relative magnitudes of these opposing physiological and mechanical effects will determine the net effect on respiratory function in health and disease.

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“…9,10,[24][25][26]34,35,40 There is growing evidence that lung permeability should be considered as a target for new therapy in ALI/ARDS: current knowledge on catecholamines-induced improved fluid clearance, 10,24,[44][45][46] trends for increase of ventilator-free days with decrease in extravascular lung water, 46 and evidence for reduction of ventilatory needs with conservative vs liberal fluid resuscitation. 47 However, validated and reliable procedures for lung permeability assessment are still lacking, although FITC-dextran 48 and semiquantitative double-isotope imaging technique (using albumin and transferrin) 49 have become popular experimentally, in vivo as well as ex vivo.…”

Section: Lung Cell Apoptosismentioning

confidence: 99%

In vivo intravital endoscopic confocal fluorescence microscopy of normal and acutely injured rat lungs

Chagnon

Fournier

Charette

et al. 2010

Laboratory Investigation

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We present a new lung imaging technique based on endoscopic confocal fluorescence microscopy (ECFM), which is a new method that is able to provide cellular and structural assessment of living tissue using a small confocal probe in direct contact with the visceral pleura. To observe distal airspace structure and cellular condition in normal and injured lungs (hyperoxic and bleomycin challenged), we used fluorescent-specific marker contrast and ECFM. Alveolar space ECFM with spectral analyses were performed at 488-nm excitation using FITC-labeled markers or naturally fluorescent dyes. The normal lung was compared with the sick lung, where our in vivo imaging experiments correlated well with results obtained with corresponding ex vivo conventional assays. Four main elements pertaining to the acute lung injury/ acute respiratory distress syndrome (ALI/ARDS) pathophysiology and established early key events were specifically studied: alveolar epithelial membrane phenotype, lung cell apoptosis, neutrophil recruitment, and edema. ECFM allowed visualization of (i) fine-tuned ultrastructural lectin (RCA-1) and sialoglycoprotein (RTI40) epithelial cell membrane expression, (ii) YO-PRO-1-related DNA linking of lung cell apoptosis, (iii) PKH2 green fluorescent cell linker-labeled neutrophil tracking in lung microcirculatory network and airspaces, (iv) FITC-dextran plasma contrast and extravasation with edema formation. ECFM provides reliable results to corresponding ex vivo fluorescent methods. ECFM, using the minimally invasive Five-1s optical instrument and specific fluorescent markers, is able to provide real-time potentially useful imaging of live unfixed normal and injured lung tissue with promising developments for improving bedside diagnostic and decision-making therapeutic strategy in patients with ALI.

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Evaluation of two-way protein fluxes across the alveolo-capillary membrane by scintigraphy in rats: effect of lung inflation

Cited by 31 publications

References 52 publications

Modeling the time-course of ventilator-induced lung injury: what can we learn from interspecies discrepancies?

Modeling the time-course of ventilator-induced lung injury: what can we learn from interspecies discrepancies?

The mechanism of deep inspiration-induced bronchoprotection: evidence from a mouse model

In vivo intravital endoscopic confocal fluorescence microscopy of normal and acutely injured rat lungs

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