High lung volume increases stress failure in pulmonary capillaries

Fu, Zhenxing; Costello, Michael L.; Tsukimoto, K.; Prediletto, Renato; Elliott, A. R.; Mathieu-Costello, Odile; West, John B.

doi:10.1152/jappl.1992.73.1.123

Cited by 292 publications

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“…Widespread endothelial and epithelial cell injury is one of the hallmarks of the entity and accounts at least in part for the increased microvascular permeability of ventilator-injured lungs (19)(20)(21)(22). Gajic and coworkers have provided direct evidence that the VILI lesion is associated with a transient loss of endothelial and/or epithelial plasma membrane integrity (23).…”

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confidence: 99%

Hypercapnic Acidosis Impairs Plasma Membrane Wound Resealing in Ventilator-injured Lungs

Doerr

Gajić

Berríos

et al. 2005

Am J Respir Crit Care Med

118

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The objective of this study was to assess the effects of hypercapnic acidosis on lung cell injury and repair by confocal microscopy in a model of ventilator-induced lung injury. Three groups of normocapnic, hypocapnic, and hypercapnic rat lungs were perfused ex vivo, either during or after injurious ventilation, with a solution containing the membrane-impermeant label propidium iodide. In lungs labeled during injurious ventilation, propidium iodide fluorescence identifies all cells with plasma membrane wounds, both permanent and transient, whereas in lungs labeled after injurious ventilation propidium iodide fluorescence identifies only cells with permanent plasma membrane wounds. Hypercapnia minimized the adverse effects of high-volume ventilation on vascular barrier function, whereas hypocapnia had the opposite effect. Despite CO 2 -dependent differences in lung mechanics and edema the number of injured subpleural cells per alveolus was similar in the three groups (0.48 Ϯ 0.34 versus 0.51 Ϯ 0.19 versus 0.43 Ϯ 0.20 for hypocapnia, normocapnia, and hypercapnia, respectively). However, compared with normocapnia the probability of wound repair was significantly reduced in hypercapnic lungs (63 versus 38%; p Ͻ 0.02). This finding was subsequently confirmed in alveolar epithelial cell scratch models. The potential relevance of these observations for lung inflammation and remodeling after mechanical injury is discussed.Keywords: permissive hypercapnia; plasma membrane wounding and repair; ventilator-induced lung injury So-called lung protective mechanical ventilation strategies emphasize lung recruitment and the avoidance of large tidal volumes. Such strategies are often associated with hypercapnic acidosis. Many experts view "permissive hypercapnia" as a necessary evil of a low tidal ventilation strategy (1). Concern about detrimental effects of acidemia on renal and cardiovascular function have motivated attempts to enhance CO 2 removal by tracheal gas insufflation (2) and have led to unsubstantiated recommendations about the use of bicarbonate buffers in hypercapnic patients (3). More recent data suggest that hypercapnia may actually protect the lung from certain manifestations of ischemiareperfusion, endotoxin, and mechanical ventilation-related injury (4-9). Hypocapnia, in contrast, and correction of acidemia may be harmful (10-12). The specific mechanisms through which hypercapnia influences lung injury and vascular barrier function remain uncertain (13). CO 2 generates H ϩ ions, which react with titratable groups in certain amino acids and/or interacts directly (Received in original form September 3, 2003; accepted in final form January 21, 2005) Supported by grants from the National Institutes of Health (HL-63178), GlaxoSmithKline, and the Brewer Foundation. with free amine groups in proteins to form carbamate residues (14-16). CO 2 -dependent effects on the generation of reactive oxygen species and reactive nitrogen species as well as effects on ion channel conductivity have all been considered (17, 18).V...

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mentioning

confidence: 99%

Hypercapnic Acidosis Impairs Plasma Membrane Wound Resealing in Ventilator-injured Lungs

Doerr

Gajić

Berríos

et al. 2005

Am J Respir Crit Care Med

118

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“…6 A ventilation strategy that avoids volutrauma, atelectrauma and biotrauma in the treatment of patients with diseases of abnormal lung compliance, such as ARDS, is firmly based on experimental literature and clinical experience. [2][3][4][5]28,30,32 The application of a lung protective strategy incorporating reduced tidal volumes, effective lung recruitment, adequate PEEP to minimize alveolar collapse during expiration and permissive hypercapnia has been shown to be advantageous in adult patients with ARDS, 5 although it has not been systematically studied in children.…”

Section: Discussionmentioning

confidence: 99%

“…[2][3][4] In contrast, a strategy that incorporates the basic principles of lung protective ventilation can hasten recovery and minimize pulmonary morbidity with its attendant mortality. 5 …”

Section: S100mentioning

confidence: 99%

“…4 The use of a mechanical ventilation strategy that causes volutrauma (high tidal volume) and atelectrauma (zero PEEP) has been shown to promote the release of inflammatory mediators such as tumor necrosis factor alpha (TNF-α). 32 This is in sharp contrast to the attenuated release of such mediators when a protective strategy with reduced tidal volume and high PEEP is employed.…”

Section: Biotraumamentioning

confidence: 99%

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Ventilação mecânica convencional em pediatria

Rotta¹,

Steinhorn²

2007

J. Pediatr. (Rio J.)

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Objective: To review the various challenges of providing mechanical ventilation to pediatric patients with diseases of increased airway resistance, diseases of abnormal lung compliance or normal lungs. Sources:Original data from our pediatric intensive care unit and animal research laboratory. Relevant articles included in the MEDLINE electronic database during the last 10 years. Also included were book chapters and definitive studies, as judged by the authors, in the fields of asthma, acute respiratory distress syndrome, mechanical ventilation, ventilator-induced lung injury and permissive hypercapnia. Summary of the findings:Mechanical ventilation of patients with diseases of increased airway resistance should center on avoidance of dynamic hyperinflation, allowing complete exhalation prior to the initiation of a subsequent breath and permissive hypercapnia. Positive end-expiratory pressure should be used sparingly to prevent atelectasis and facilitate synchrony in spontaneously breathing patients. Mechanical ventilation of patients with diseases of abnormal lung compliance should take into consideration the inhomogeneous distribution of lung disease. Focus should be on avoidance of volutrauma and atelectrauma that could result in ventilator-associated lung injury. Conclusions:The last decade was marked by significant advances in the management of pediatric respiratory failure. The choice of mechanical ventilation strategy can significantly influence the subsequent course of lung injury.Mechanical ventilation can no longer be viewed simply as a harmless support modality that is employed to keep patients alive while disease-specific treatments are used to ameliorate the underlying pathology.J Pediatr (Rio J). 2007;83(2 Suppl):S100-108: Mechanical ventilation, acute lung injury, acute respiratory distress syndrome, status asthmaticus, permissive hypercapnia.

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“…Moreover, overinflation of the remaining lung may induce an associated epithelial injury. It has been demonstrated that stress failure occurs more frequently at high than at low lung volumes for a given transmural pressure [28]. There is a spectrum from low-reversible, permeability oedema [29] to high-, probably more irreversible, permeability oedema [30], as the transmural pressure is raised.…”

Section: P Bauermentioning

confidence: 99%

Postpneumonectomy pulmonary oedema revisited

Bauer¹

2000

Eur Respir J

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Postoperative pulmonary oedema occurs early postoperatively (>6 h) and is associated with a net fluid overload. A recent survey of 8,195 major operations showed an incidence of 7.6%, with a mortality of 11.9% [1]. Postpneumonectomy pulmonary oedema (PPO) occurs after pneumonectomy [2] or lung resection [3], in the absence of left ventricular dysfunction or infection. The overall incidence is 5.1% with a mortality of 3.6% [4].Although PPO has not yet been well defined, there is a growing body of evidence suggesting that increased pulmonary perfusion flow and the subsequent rise in net filtration pressure [5], a restricted capillary volume [2], endothelial damage, amputation of the lymphatic system [6] and hyperinflation [7] are the main causes of this poorly understood clinical entity [8].PPO occurs more often after pneumonectomy than after partial lung resection and right pneumonectomy seems to be more frequently involved [9,10]. Prior radiotherapy and intraoperative fluid overload are independent risk factors in cancer patients [3]. Transfusion of fresh frozen plasma and higher mechanical ventilation pressures during surgery are also independent factors [11].Prognosis varies according to the presentation. Although some studies report a high mortality (~100%) [12], others found different degrees of lung impairment, from acute lung injury (mild-to-moderate) to adult respiratory distress syndrome (ARDS) (severe), the latter being associated with a poor prognosis [3,4,11].Experimental and clinical studies suggest that factors other than fluid overload contribute to disease severity [10]. In dogs, pneumonectomy does not acutely increase susceptibility to extravascular lung water formation (EVLW) caused by haemodynamic challenge [13]. PPO occurs after contralateral pneumonectomy and mediastinal lymphatic interruption [6]. The simple procedure of thoracotomy results in an increase in EVLW, and the addition of manual compression of the lung facilitates this increase in EVLW even further [14]. Postoperative pulmonary function, assessed by means of the forced expiratory volume in one second, is reduced for $2 weeks, irrespective of the extent of pulmonary resection [15]. Pulmonary endothelial permeability is increased after pneumonectomy [16,17]. All these data suggest that the pulmonary blood/gas barrier is somewhat altered in PPO because of endothelial or epithelial injury, or both.In this issue of the European Respiratory Journal, JORDAN et al.[18] present a review of PPO with emphasis on some hypotheses regarding its pathogenesis. Among different pathogenic factors, the authors focus on the role played by ischaemia, or more precisely hypoxaemia, and reperfusion injury of the remaining lung. In the experimental model of ischaemia/reperfusion of the lungs, an imbalance between intracellular generation of toxic oxidants [19] and reduced nitric oxide production [20,21] triggers an inflammatory response. Neutrophils begin rolling along and sticking to the vascular endothelium of the postcapillary venules, and migrate to ...

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High lung volume increases stress failure in pulmonary capillaries

Cited by 292 publications

References 0 publications

Hypercapnic Acidosis Impairs Plasma Membrane Wound Resealing in Ventilator-injured Lungs

Hypercapnic Acidosis Impairs Plasma Membrane Wound Resealing in Ventilator-injured Lungs

Ventilação mecânica convencional em pediatria

Postpneumonectomy pulmonary oedema revisited

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