- Chemokine Involvement in Lung Injury Secondary to Ischaemia/Reperfusion. [Journal Article]
- LUNGLung 2017 Apr 21
- CONCLUSIONS: The present study demonstrates that activated neutrophils, as well as MCP-1, MIP-2, and ICAM-1, are involved in inflammatory response induced by ischaemia-reperfusion-induced lung injury.
- Risk factors for noninvasive ventilation failure in patients with acute cardiogenic pulmonary edema: A prospective, observational cohort study. [Letter]
- JCJ Crit Care 2017 Apr 13
- Sevoflurane Posttreatment Attenuates Lung Injury Induced by Oleic Acid in Dogs. [Journal Article]
- A&AAnesth Analg 2017; 124(5):1555-1563
- CONCLUSIONS: When compared with propofol, sevoflurane attenuates OA-induced lung damage. However, despite this effect on lung histology and inflammation, sevoflurane worsened oxygenation in OA-induced ALI, possibly via inhibition of hypoxic pulmonary vasoconstriction.
- Hydroxytyrosol attenuates LPS-induced acute lung injury in mice by regulating autophagy and sirtuin expression. [Journal Article]
- CMCurr Mol Med 2017 Apr 21
- CONCLUSIONS: The protective effect of HT on lung inflammation in ALI mice may be attributed to the promotion of autophagy, which is likely associated with the activation of the SIRT/MAPK signaling pathway. Importantly, this study provides new insight into the molecular mechanisms of HT and its therapeutic potential in the treatment of acute respiratory distress syndrome.
- High-Fat Feeding Protects Mice From Ventilator-Induced Lung Injury, Via Neutrophil-Independent Mechanisms. [Journal Article]
- CCCrit Care Med 2017 Apr 19
- CONCLUSIONS: Consumption of a high-fat diet protects mice from ventilator-induced lung injury in a manner independent of neutrophil recruitment, which we postulate instead arises through blunted up-regulation of CD147 expression and subsequent activation of intra-alveolar matrix metalloproteinases. These findings may open avenues for therapeutic manipulation in acute respiratory distress syndrome and could have implications for understanding the pathogenesis of lung disease in obese patients.
- Protective Effects of Li-Fei-Xiao-Yan Prescription on Lipopolysaccharide-Induced Acute Lung Injury via Inhibition of Oxidative Stress and the TLR4/NF-κB Pathway. [Journal Article]
- EBEvid Based Complement Alternat Med 2017; 2017:1791789
- Li-Fei-Xiao-Yan prescription (LFXY) has been clinically used in China to treat inflammatory and infectious diseases including inflammatory lung diseases. The present study was aimed at evaluating the...
Li-Fei-Xiao-Yan prescription (LFXY) has been clinically used in China to treat inflammatory and infectious diseases including inflammatory lung diseases. The present study was aimed at evaluating the potential therapeutic effects and potential mechanisms of LFXY in a murine model of lipopolysaccharide- (LPS-) induced acute lung injury (ALI). In this study, the mice were orally pretreated with LFXY or dexamethasone (positive drug) before the intratracheal instillation of LPS. Our data indicated that pretreatment with LFXY enhanced the survival rate of ALI mice, reversed pulmonary edema and permeability, improved LPS-induced lung histopathology impairment, suppressed the excessive inflammatory responses via decreasing the expression of proinflammatory cytokines (TNF-α, IL-1β, and IL-6) and chemokine (MIP-2) and inhibiting inflammatory cells migration, and repressed oxidative stress through the inhibition of MPO and MDA contents and the upregulation of antioxidants (SOD and GSH) activities. Mechanistically, treatment with LFXY significantly prevented LPS-induced TLR4 expression and NF-κB (p65) phosphorylation. Overall, the present study suggests that LFXY protected mice from acute lung injury induced by LPS via inhibition of TLR4/NF-κB p65 activation and upregulation of antioxidative enzymes and it may be a potential preventive and therapeutic agent for ALI in the clinical setting.
- Interleukin-6 displays lung anti-inflammatory properties and exerts protective hemodynamic effects in a double-hit murine acute lung injury. [Journal Article]
- RRRespir Res 2017 Apr 19; 18(1):64
- CONCLUSIONS: In a double-hit murine model of ARDS, IL-6 deficient mice experienced more severe bronchoalveolar cellular inflammation as compared to wild-type littermates. Furthermore, IL-6 deficiency caused marked acute pulmonary hypertension, which may be, at least partially, due to vasoactive mechanisms. A dysregulation of nitric oxide synthase may account for this observation, a hypothesis that will need to be investigated in future studies.
- Chronic Atrial Fibrillation Ablation with Harmonic Scalpel during Mitral Valve Surgery. [Journal Article]
- BJBraz J Cardiovasc Surg 2017 Jan-Feb; 32(1):22-28
- CONCLUSIONS: Surgical treatment of chronic atrial fibrillation with ultrasound concomitant with mitral valve surgery is feasible and satisfactory, with maintenance of sinus rhythm in most patients (83.8%) after 60 months of follow-up.
- Incidence and Implications of Left Ventricular Distention During Venoarterial Extracorporeal Membrane Oxygenation Support. [Journal Article]
- AJASAIO J 2017 Apr 12
- Left ventricular distention (LVD) during venoarterial extracorporeal membrane oxygenation (VA-ECMO) support is increasingly recognized but seldom reported in the literature. The present study defined...
Left ventricular distention (LVD) during venoarterial extracorporeal membrane oxygenation (VA-ECMO) support is increasingly recognized but seldom reported in the literature. The present study defined LVD as not present (LVD-); subclinical (LVD+, evidence of pulmonary edema on chest radiograph AND pulmonary artery diastolic blood pressure greater than 25 mmHg within the first 2 hours of ICU admission); or clinical (LVD++, need for decompression of the left ventricle immediately following VA-ECMO initiation). Among 226 VA-ECMO device runs, 121 had sufficient data to define LVD retrospectively. Nine patients (7%) developed LVD++ requiring immediate decompression, and 27 patients (22%) met the definition of LVD+. Survival to discharge was similar among groups (LVD++: 44%, LVD+: 41%, LVD-: 44%). However, myocardial recovery appeared inversely related to degree of LVD (LVD++: 11%, LVD+: 26%, LVD-: 40%). When death or transition to device was considered as a composite outcome, event-free survival was diminished in LVD++ and LVD+ patients as compared to LVD-. Multivariable analysis identified cannulation of VA-ECMO during CPR (ECPR) as a risk factor for decompression (OR: 3.64, CI: 1.21 - 10.98, p=0.022). Using a novel definition of LVD, the severity LVD was inversely related to the likelihood of myocardial recovery. Survival did not differ between groups. ECPR was associated with need for mechanical intervention.
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- Hemin Causes Lung Microvascular Endothelial Barrier Dysfunction by Necroptotic Cell Death. [Journal Article]
- AJAm J Respir Cell Mol Biol 2017 Apr 19
- Hemin, the oxidized prosthetic moiety of hemoglobin, has been implicated in the pathogenesis of acute chest syndrome (ACS) in sickle cell patients by virtue of its endothelial-activating properties. ...
Hemin, the oxidized prosthetic moiety of hemoglobin, has been implicated in the pathogenesis of acute chest syndrome (ACS) in sickle cell patients by virtue of its endothelial-activating properties. In this study, we examined whether hemin can cause lung microvascular endothelial barrier dysfunction. By assessing transendothelial resistance using electrical cell impedance sensing, and by directly measuring trans-monolayer FITC-dextran flux, we found that hemin does cause endothelial barrier dysfunction in a concentration-dependent manner. Pre-treatment with either a TLR4 inhibitor, TAK-242, or an antioxidant, N-acetylcysteine, abrogated this effect. Increased monolayer permeability was found to be associated with programmed cell death by necroptosis as evidenced by Trypan blue staining, TUNEL assay, Western blotting for activated forms of key effectors of cell death pathways, and studies utilizing specific inhibitors of necroptosis and apoptosis. Further study examining the role of EC necroptosis in promoting non-cardiogenic pulmonary edema during ACS is warranted, and may open a new avenue of potential treatment for this devastating disease.