The Effects of Low and High Tidal Volume and Pentoxifylline on Intestinal Blood Flow and Leukocyte-Endothelial Interactions in Mechanically Ventilated Rats

Aikawa, Priscila; Zhang, Haibo; Barbas, Carmen Sílvia Valente; Pazetti, Rogério; Correia, Cristiano de Jesus; Mauad, Thaís; Silva, Eliezer; Sannomiya, Paulina; Poli-de-Figueiredo, Luiz Francisco; Nakagawa, Naomi Kondo

doi:10.4187/respcare.01183

Cited by 5 publications

(4 citation statements)

References 38 publications

(69 reference statements)

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“…In this context, it is not surprising that despite reducing NM-mediated inflammation, pentoxifylline has little effect on NM-mediated changes in pulmonary mechanics. Earlier studies have shown a protective effect of pentoxifylline against altered lung function induced experimentally by mechanical ventilation or recurrent airway obstruction, and in humans with sarcoidosis or after smoke inhalation (Aikawa et al, 2011; Leguillette et al, 2002; Ogura et al, 1994; Zabel et al, 1997). However, these studies focused on oxygenation and overall inflammatory cell recruitment to the lung.…”

Section: Discussionmentioning

confidence: 99%

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation

Sunil

Vayas

Cervelli

et al. 2014

Experimental and Molecular Pathology

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Nitrogen mustard (NM) is a toxic alkylating agent that causes damage to the respiratory tract. Evidence suggests that macrophages and inflammatory mediators including tumor necrosis factor (TNF)α contribute to pulmonary injury. Pentoxifylline is a TNFα inhibitor known to suppress inflammation. In these studies, we analyzed the ability of pentoxifylline to mitigate NM-induced lung injury and inflammation. Exposure of male Wistar rats (250 g; 8–10 weeks) to NM (0.125 mg/kg, i.t.) resulted in severe histolopathological changes in the lung within 3 d of exposure, along with increases in bronchoalveolar lavage (BAL) cell number and protein, indicating inflammation and alveolar-epithelial barrier dysfunction. This was associated with increases in oxidative stress proteins including lipocalin (Lcn)2 and heme oxygenase (HO)-1 in the lung, along with pro-inflammatory/cytotoxic (COX-2+ and MMP-9+), and anti-inflammatory/wound repair (CD163+ and Gal-3+) macrophages. Treatment of rats with pentoxifylline (46.7 mg/kg, i.p.) daily for 3 d beginning 15 min after NM significantly reduced NM-induced lung injury, inflammation, and oxidative stress, as measured histologically and by decreases in BAL cell and protein content, and levels of HO-1 and Lcn2. Macrophages expressing COX-2 and MMP-9 also decreased after pentoxifylline, while CD163+ and Gal-3+ macrophages increased. This was correlated with persistent upregulation of markers of wound repair including pro-surfactant protein-C and proliferating nuclear cell antigen by Type II cells. NM-induced lung injury and inflammation were associated with alterations in the elastic properties of the lung, however these were largely unaltered by pentoxifylline. These data suggest that pentoxifylline may be useful in treating acute lung injury, inflammation and oxidative stress induced by vesicants.

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Section: Discussionmentioning

confidence: 99%

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation

Sunil

Vayas

Cervelli

et al. 2014

Experimental and Molecular Pathology

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“…Systemic mean arterial blood pressure (MABP) and heart rate (HR) were continuously monitored through acquisition system instruments (MP 100, BIOPAC system Inc.) and recorded via computer (Chart 4 record system; Biopack Systems Inc., Santa Barbara, CA). In addition, a cannula was inserted into the trachea [ 5 , 23 ] and a G5 ventilator (Hamilton Medical AG, Switzerland) was used and connected to an end tidal expiratory CO 2 monitor (PETCO 2 ; Hamilton Medical AG, Switzerland).…”

Section: Methodsmentioning

confidence: 99%

“…Lung tissues in formalin-fixed paraffin sections (4-μm) were stained with hematoxylin and eosin (H&E, X 400) [ 5 , 23 ]. In addition, unstained sections were deparaffinized before antigen retrieval and endogenous peroxidase was blocked using 3% H 2 O 2 in methanol for 15 min.…”

Section: Methodsmentioning

confidence: 99%

Membrane Translocation of IL-33 Receptor in Ventilator Induced Lung Injury

Yang

Lin

et al. 2015

PLoS ONE

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Ventilator-induced lung injury is associated with inflammatory mechanism and causes high mortality. The objective of this study was to discover the role of IL-33 and its ST2 receptor in acute lung injury induced by mechanical ventilator (ventilator-induced lung injury; VILI). Male Wistar rats were intubated after tracheostomy and received ventilation at 10 cm H2O of inspiratory pressure (PC10) by a G5 ventilator for 4 hours. The hemodynamic and respiratory parameters were collected and analyzed. The morphological changes of lung injury were also assessed by histological H&E stain. The dynamic changes of lung injury markers such as TNF-α and IL-1β were measured in serum, bronchoalveolar lavage fluid (BALF), and lung tissue homogenization by ELISA assay. During VILI, the IL-33 profile change was detected in BALF, peripheral serum, and lung tissue by ELISA analysis. The Il-33 and ST2 expression were analyzed by immunohistochemistry staining and western blot analysis. The consequence of VILI by H&E stain showed inducing lung congestion and increasing the expression of pro-inflammatory cytokines such as TNF-α and IL-1β in the lung tissue homogenization, serum, and BALF, respectively. In addition, rats with VILI also exhibited high expression of IL-33 in lung tissues. Interestingly, the data showed that ST2L (membrane form) was highly accumulated in the membrane fraction of lung tissue in the PC10 group, but the ST2L in cytosol was dramatically decreased in the PC10 group. Conversely, the sST2 (soluble form) was slightly decreased both in the membrane and cytosol fractions in the PC10 group compared to the control group. In conclusion, these results demonstrated that ST2L translocation from the cytosol to the cell membranes of lung tissue and the down-expression of sST2 in both fractions can function as new biomarkers of VILI. Moreover, IL-33/ST2 signaling activated by mechanically responsive lung injury may potentially serve as a new therapy target.

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“…Applying the optimal level of Positive End Expiratory Pressure (PEEP) is the main component in the treatment of Acute Respiratory Distress Syndrome (ARDS) [1]. Optimal PEEP is the value that ensures the best lung recruitment, resulting in enhancement of oxygenation without lung hyperinflation or affection of hemodynamics [2].…”

Section: Introductionmentioning

confidence: 99%

Lung ultrasound- versus FiO₂-guided PEEP in ARDS patients

Salem

Eltatawy

Abdelhafez

et al. 2020

Egyptian Journal of Anaesthesia

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Background: Although FiO 2-determined PEEP is the standard in ARDS management, previous trials failed to show agreement on outcomes. Based on heterogeneous ARDS pathology, we evaluated the effect of LUS-determined PEEP on oxygenation and outcomes. Methods: In this prospective, controlled trial, we randomly assigned 60 patients into LUSdetermined PEEP (group l) and FiO 2-determined PEEP (group II). LUS-determined PEEP was based on LUS aeration score. Primary outcome was P/F ratio, secondary outcomes were; static compliance, 28-day mortality, duration of MV and length of ICU-stay. Results: P/F ratio was 266 ± 44.5 in group I, 233 ± 53.9 in group II. Static compliance was 54.8 ± 6.6 in group I, 45.9 ± 3.8 in group II. IQR of duration of MV was 4-6 with a median value of 5 in group l, 6-11.7 with a median value of 7.5 in group ll. 28-day mortality was 6.7% in group l, 30% in group ll. The relative risk of mortality in group II is more or less 5 times in group I (RR 4.87 with 95%CI of 1.492-15.893). IQR of organ dysfunction-free days was 16-19 with a median value of 18 in group l, 0-12 with a median value of 10 in group ll. IQR of MV-free days was 22-24 with a median value of 23 in group l, 0-22 with a median value of 20 in group ll. Conclusion: LUS-guided PEEP showed improved oxygenation, compliance and decreased mortality, organ dysfunction, duration of MV and ICU compared with FiO 2-guided PEEP.

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The Effects of Low and High Tidal Volume and Pentoxifylline on Intestinal Blood Flow and Leukocyte-Endothelial Interactions in Mechanically Ventilated Rats

Cited by 5 publications

References 38 publications

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation

Membrane Translocation of IL-33 Receptor in Ventilator Induced Lung Injury

Lung ultrasound- versus FiO₂-guided PEEP in ARDS patients

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The Effects of Low and High Tidal Volume and Pentoxifylline on Intestinal Blood Flow and Leukocyte-Endothelial Interactions in Mechanically Ventilated Rats

Cited by 5 publications

References 38 publications

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation

Pentoxifylline attenuates nitrogen mustard-induced acute lung injury, oxidative stress and inflammation

Membrane Translocation of IL-33 Receptor in Ventilator Induced Lung Injury

Lung ultrasound- versus FiO2-guided PEEP in ARDS patients

Contact Info

Product

Resources

About

Lung ultrasound- versus FiO₂-guided PEEP in ARDS patients