Pentraxin 3 accelerates lung injury in high tidal volume ventilation in mice

2012 ◽  
Vol 51 (1) ◽  
pp. 82-90 ◽  
Author(s):  
Juliana Monte Real ◽  
Graziela Machado Gruner Turco Spilborghs ◽  
Mariana Morato-Marques ◽  
Ricardo Pereira de Moura ◽  
Elnara Marcia Negri ◽  
...  
Keyword(s):  
Lung Injury ◽  
Tidal Volume ◽  
High Tidal Volume ◽  
Pentraxin 3 ◽  
High Tidal Volume Ventilation ◽  
Volume Ventilation

High tidal volume ventilation induces NOS2 and impairs cAMP- dependent air space fluid clearance

2003 ◽  
Vol 284 (5) ◽  
pp. L791-L798 ◽  
Author(s):  
James A. Frank ◽  
Jean-François Pittet ◽  
Hyon Lee ◽  
Micaela Godzich ◽  
Michael A. Matthay
Keyword(s):  
Lung Injury ◽  
Tidal Volume ◽  
Time Course ◽  
High Tidal Volume ◽  
Low Tidal Volume ◽  
Edema Fluid ◽  
High Tidal Volume Ventilation ◽  
Volume Ventilation ◽  
Air Space ◽  
Induced Changes

Tidal volume reduction during mechanical ventilation reduces mortality in patients with acute lung injury and the acute respiratory distress syndrome. To determine the mechanisms underlying the protective effect of low tidal volume ventilation, we studied the time course and reversibility of ventilator-induced changes in permeability and distal air space edema fluid clearance in a rat model of ventilator-induced lung injury. Anesthetized rats were ventilated with a high tidal volume (30 ml/kg) or with a high tidal volume followed by ventilation with a low tidal volume of 6 ml/kg. Endothelial and epithelial protein permeability were significantly increased after high tidal volume ventilation but returned to baseline levels when tidal volume was reduced. The basal distal air space fluid clearance (AFC) rate decreased by 43% ( P < 0.05) after 1 h of high tidal volume but returned to the preventilation rate 2 h after tidal volume was reduced. Not all of the effects of high tidal volume ventilation were reversible. The cAMP-dependent AFC rate after 1 h of 30 ml/kg ventilation was significantly reduced and was not restored when tidal volume was reduced. High tidal volume ventilation also increased lung inducible nitric oxide synthase (NOS2) expression and air space total nitrite at 3 h. Inhibition of NOS2 activity preserved cAMP-dependent AFC. Because air space edema fluid inactivates surfactant and reduces ventilated lung volume, the reduction of cAMP-dependent AFC by reactive nitrogen species may be an important mechanism of clinical ventilator-associated lung injury.

scholarly journals High tidal volume ventilation does not exacerbate acid-induced lung injury in infant rats

2013 ◽  
Vol 189 (1) ◽  
pp. 129-135 ◽  
Author(s):  
Peter D. Sly ◽  
Philip K. Nicholls ◽  
Luke J. Berry ◽  
Zoltán Hantos ◽  
Vincenzo Cannizzaro
Keyword(s):  
Lung Injury ◽  
Tidal Volume ◽  
High Tidal Volume ◽  
Infant Rats ◽  
High Tidal Volume Ventilation ◽  
Volume Ventilation

scholarly journals Rap1 mediates protective effects of iloprost against ventilator-induced lung injury

2009 ◽  
Vol 107 (6) ◽  
pp. 1900-1910 ◽  
Author(s):  
Anna A. Birukova ◽  
Panfeng Fu ◽  
Junjie Xing ◽  
Konstantin G. Birukov
Keyword(s):  
Lung Injury ◽  
Bronchoalveolar Lavage ◽  
Tidal Volume ◽  
Evans Blue ◽  
High Tidal Volume ◽  
Protective Effects ◽  
Ventilator Induced Lung Injury ◽  
High Tidal Volume Ventilation ◽  
Volume Ventilation

Prostaglandin I2 (PGI2) has been shown to attenuate vascular constriction, hyperpermeability, inflammation, and acute lung injury. However, molecular mechanisms of PGI2 protective effects on pulmonary endothelial cells (EC) are not well understood. We tested a role of cAMP-activated Epac-Rap1 pathway in the barrier protective effects of PGI2 analog iloprost in the murine model of ventilator-induced lung injury. Mice were treated with iloprost (2 μg/kg) after onset of high tidal volume ventilation (30 ml/kg, 4 h). Bronchoalveolar lavage, histological analysis, and measurements of Evans blue accumulation were performed. In vitro, microvascular EC barrier function was assessed by morphological analysis of agonist-induced gap formation and monitoring of Rho pathway activation and EC permeability. Iloprost reduced bronchoalveolar lavage protein content, neutrophil accumulation, capillary filtration coefficient, and Evans blue albumin extravasation caused by high tidal volume ventilation. Small-interfering RNA-based Rap1 knockdown inhibited protective effects of iloprost. In vitro, iloprost increased barrier properties of lung microvascular endothelium and alleviated thrombin-induced EC barrier disruption. In line with in vivo results, Rap1 depletion attenuated protective effects of iloprost in the thrombin model of EC permeability. These data describe for the first time protective effects for Rap1-dependent signaling against ventilator-induced lung injury and pulmonary endothelial barrier dysfunction.

High tidal volume ventilation induces lung injury after hepatic ischemia-reperfusion

2007 ◽  
Vol 292 (3) ◽  
pp. L625-L631 ◽  
Author(s):  
Shuhei Ota ◽  
Kyota Nakamura ◽  
Takuya Yazawa ◽  
Yosuke Kawaguchi ◽  
Yasuko Baba ◽  
...  
Keyword(s):  
Lung Injury ◽  
Tidal Volume ◽  
Ischemia Reperfusion ◽  
Weight Ratio ◽  
High Tidal Volume ◽  
Sham Operation ◽  
Liver Ischemia ◽  
High Tidal Volume Ventilation ◽  
Volume Ventilation ◽  
Tnf Α

Ischemia-reperfusion not only damages the affected organ but also leads to remote organ injuries. Hepatic inflow interruption usually occurs during hepatic surgery. To investigate the influence of liver ischemia-reperfusion on lung injury and to determine the contribution of tidal volume settings on liver ischemia-reperfusion-induced lung injury, we studied anesthetized and mechanically ventilated rats in which the hepatic inflow was transiently interrupted twice for 15 min. Two tidal volumes, 6 ml/kg as a low tidal volume (IR-LT) and 24 ml/kg as a high tidal volume (IR-HT), were assessed after liver ischemia-reperfusion, as well as after a sham operation, 6 ml/kg (NC-LT) and 24 ml/kg (NC-HT). Both the IR-HT and IR-LT groups had a gradual decline in the systemic blood pressure and a significant increase in plasma TNF-α concentrations. Of the four groups, only the IR-HT group developed lung injury, as assessed by an increase in the lung wet-to-dry weight ratio, the presence of significant histopathological changes, such as perivascular edema and intravascular leukocyte aggregation, and an increase in the bronchoalveolar lavage fluid TNF-α concentration. Furthermore, only in the IR-HT group was airway pressure increased significantly during the 6-h reperfusion period. These findings suggest that liver ischemia-reperfusion caused systemic inflammation and that lung injury is triggered when high tidal volume ventilation follows liver ischemia-reperfusion.

scholarly journals Effects of high-tidal-volume mechanical ventilation on the expression of P2X7 receptor and inflammatory response in lung tissue of rats

2018 ◽  
Vol 16 ◽  
pp. 205873921879594
Author(s):  
Jia Jia ◽  
Hanyu Qin ◽  
Bin Zang
Keyword(s):  
Mechanical Ventilation ◽  
Lung Injury ◽  
Tidal Volume ◽  
Lung Tissue ◽  
Sham Group ◽  
Receptor Expression ◽  
High Tidal Volume ◽  
Caspase 1 ◽  
High Tidal Volume Ventilation ◽  
Volume Ventilation

Ventilator-induced lung injury is a severe complication mainly caused from mechanical ventilation (MV), associated with the upregulation of inflammation response. The mechanism still remains unclear. This study aims to explore the effects of pathological damage, neutrophil infiltration, expression of P2X7 receptor, and activation of Caspase-1 in lung tissue using a rat model. Sprague Dawley (SD) rats were randomly divided into sham group, conventional MV group, and high-tidal-volume ventilation group and fed with clean water and rat food. The sham group received tracheotomy without MV; conventional MV group was given 7 mL/kg tidal volume ventilation, and high-tidal-volume MV group was given 28 mL/kg tidal volume ventilation. All the rats were sacrificed after 4 h of ventilation or spontaneous breath. Lung wet/dry ratio was measured, and paraffin sections were prepared for pathological injury assessment and immunohistochemistry of P2X7 and myeloperoxidase levels. Lung homogenate was used for Western blot analysis of P2X7 receptor and Caspase-1 levels and real-time polymerase chain reaction (PCR) analysis of P2X7 gene expression level. Compared to sham group and conventional MV group, high-tidal-volume MV led to an increase in lung wet/dry ratio and histology score. High-tidal-volume ventilation also led to chemotaxis of neutrophils. The expression levels of protein and messenger RNA (mRNA) of P2X7 receptor were significantly upregulated. Cleaved-caspase-1 expression was also upregulated. All data provide the evidence that high-tidal-volume MV can lead to lung injury, neutrophils infiltration, and upregulation of cleaved-Caspase-1 level. This result may be related to the upregulation of P2X7 receptor expression.

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