Inspiratory Resistive Breathing Induces Acute Lung Injury

Toumpanakis, Dimitris; Kastis, George A.; Zacharatos, Panagiotis; Sigala, Ioanna; Michailidou, Tatiana; Kouvela, Marousa; Glynos, Constantinos; Divangahi, Maziar; Roussos, Charis; Theocharis, Stamatios; Vassilakopoulos, Theodoros P.

doi:10.1164/rccm.201001-0116oc

Cited by 68 publications

(102 citation statements)

References 51 publications

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“…The inspiratory port was then connected to a tube of small diameter (resistance), and the diameter was adjusted to provide a peak tidal Pi of 50% of maximum IRB ( Fig. 1) (51). The inspiratory line supplied 100% oxygen throughout the period of RB so as to prevent the development of hypoxemia.…”

Section: Methodsmentioning

confidence: 99%

MAPKs and NF-κB differentially regulate cytokine expression in the diaphragm in response to resistive breathing: the role of oxidative stress

Sigala

Zacharatos²,

Toumpanakis

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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Inspiratory resistive breathing (IRB) induces cytokine expression in the diaphragm. The mechanism of this cytokine induction remains elusive. The roles of MAPKs and NF-κB and the impact of oxidative stress in IRB-induced cytokine upregulation in the diaphragm were studied. Wistar rats were subjected to IRB (50% of maximal inspiratory pressure) via a two-way nonrebreathing valve for 1, 3, or 6 h. Additional groups of rats subjected to IRB for 6 h were randomly assigned to receive either solvent or N-acetyl-cysteine (NAC) or inhibitors of NF-κB (BAY-11–7082), ERK1/2 (PD98059), and P38 MAPK (SB203580) to study the effect of oxidative stress, NF-κB, and MAPKs in IRB-induced cytokine upregulation in the diaphragm. Quietly breathing animals served as controls. IRB upregulated cytokine (IL-6, TNF-α, IL-10, IL-2, IL-1β) protein levels in the diaphragm and resulted in increased activation of MAPKs (P38, ERK1/2) and NF-κB. Inhibition of NF-κB and ERK1/2 blunted the upregulation of all cytokines except that of IL-6, which was further increased. P38 inhibition attenuated all cytokine (including IL-6) upregulation. Both P38 and ERK1/2 inhibition decreased NF-κB/p65 subunit phosphorylation. NAC pretreatment blunted IRB-induced cytokine upregulation in the diaphragm and resulted in decreased ERK1/2, P38, and NF-κB/p65 phosphorylation. In conclusion, IRB-induced cytokine upregulation in the diaphragm is under the regulatory control of MAPKs and NF-κB. IL-6 is regulated differently from all other cytokines through a P38-dependent and NF-κB independent pathway. Oxidative stress is a stimulus for IRB-induced cytokine upregulation in the diaphragm.

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Section: Methodsmentioning

confidence: 99%

MAPKs and NF-κB differentially regulate cytokine expression in the diaphragm in response to resistive breathing: the role of oxidative stress

Sigala

Zacharatos²,

Toumpanakis

et al. 2011

American Journal of Physiology-Regulatory, Integrative and Comp

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“…21 High inspiratory resistance may not only reflect differences in underlying physiology, but may relate to the pathogenesis of airway inflammation 64 and acute lung injury. 65 The methodology and analysis of FOT data are complex. The European Respiratory Society has published guidelines on methodology in 2003, 6 but there have been no updates since then.…”

Section: Measurement Of Airway Resistance By the Forced Oscillation Tmentioning

confidence: 99%

What Does Airway Resistance Tell Us About Lung Function?

2012

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SummarySpirometry is considered the primary method to detect the air flow limitation associated with obstructive lung disease. However, air flow limitation is the end-result of many factors that contribute to obstructive lung disease. One of these factors is increased airway resistance. Airway resistance is traditionally measured by relating air flow and driving pressure using body plethysmography, thus deriving airway resistance (R aw ), specific airway resistance (sR aw ), and specific airway conductance (sG aw ). Other methods to measure airway resistance include the forced oscillation technique (FOT), which allows calculation of respiratory system resistance (R RS ) and reactance (X RS ), and the interrupter technique, which allows calculation of interrupter resistance (R int ). An advantage of these other methods is that they may be easier to perform than spirometry, making them particularly suited to patients who cannot perform spirometry, such as young children, patients with neuromuscular disorders, or patients on mechanical ventilation. Since spirometry also requires a deep inhalation, which can alter airway resistance, these alternative methods may provide more sensitive measures of airway resistance. Furthermore, the FOT provides unique information about lung mechanics that is not available from analysis using spirometry, body plethysmography, or the interrupter technique. However, it is unclear whether any of these measures of airway resistance contribute clinically important information to the traditional measures derived from spirometry (FEV 1 , FVC, and FEV 1 /FVC). The purpose of this paper is to review the physiology and methodology of these measures of airway resistance, and then focus on their clinical utility in relation to each other and to spirometry.

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“…Additionally, iatrogenic pneumothorax may occur due to non-invasive diagnostic methods, such as spirometry. Breathing maneuvers with a spirometer decreases pleural pressure, increases transpulmonary pressure, and produces large negative swings in intrathoracic pressures, which is similar to the Müller maneuver (19,20). A possible complication of an abrupt increase in transpulmonary pressure is pneumothorax secondary to the barotrauma (7).…”

Section: Discussionmentioning

confidence: 99%