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endothelial damage mechanical ventilation

Florian Brettner, Vera von Dossow, Daniel Chappell
PURPOSE OF REVIEW: Ventilator-induced lung injury is a major contributor to perioperative lung injury. The end-expiratory lung volume, regional lung overdistension, and tidal recruitment are known to be the main factors causing subsequent alveolar damage and inflammation. The alveolar-capillary membrane including the endothelial glycocalyx as an integral part of the vascular endothelium seems to play a major role in different kinds of lung injury. RECENT FINDINGS: Recent studies underline the pivotal importance of the endothelial glycocalyx in lung injury...
February 2017: Current Opinion in Anaesthesiology
Gisele de A Padilha, Lucas F B Horta, Lillian Moraes, Cassia L Braga, Milena V Oliveira, Cíntia L Santos, Isalira P Ramos, Marcelo M Morales, Vera Luiza Capelozzi, Regina C S Goldenberg, Marcelo Gama de Abreu, Paolo Pelosi, Pedro L Silva, Patricia R M Rocco
BACKGROUND: In patients with emphysema, invasive mechanical ventilation settings should be adjusted to minimize hyperinflation while reducing respiratory effort and providing adequate gas exchange. We evaluated the impact of pressure-controlled ventilation (PCV) and pressure support ventilation (PSV) on pulmonary and diaphragmatic damage, as well as cardiac function, in experimental emphysema. METHODS: Emphysema was induced by intratracheal instillation of porcine pancreatic elastase in Wistar rats, once weekly for 4 weeks...
December 2016: Intensive Care Medicine Experimental
Anantha Harijith, Srikanth Pendyala, David L Ebenezer, Alison W Ha, Panfeng Fu, Yue-Ting Wang, Ke Ma, Peter T Toth, Evgeny V Berdyshev, Prasad Kanteti, Viswanathan Natarajan
Hyperoxia-induced lung injury adversely affects ICU patients and neonates on ventilator assisted breathing. The underlying culprit appears to be reactive oxygen species (ROS)-induced lung damage. The major contributor of hyperoxia-induced ROS is activation of the multiprotein enzyme complex NADPH oxidase. Sphingosine-1-phosphate (S1P) signaling is known to be involved in hyperoxia-mediated ROS generation; however, the mechanism(s) of S1P-induced NADPH oxidase activation is unclear. Here, we investigated various steps in the S1P signaling pathway mediating ROS production in response to hyperoxia in lung endothelium...
August 1, 2016: American Journal of Physiology. Lung Cellular and Molecular Physiology
Benjamin E Orwoll, Anil Sapru
Acute respiratory distress syndrome (ARDS) is common among mechanically ventilated children and accompanies up to 30% of all pediatric intensive care unit deaths. Though ARDS diagnosis is based on clinical criteria, biological markers of acute lung damage have been extensively studied in adults and children. Biomarkers of inflammation, alveolar epithelial and capillary endothelial disruption, disordered coagulation, and associated derangements measured in the circulation and other body fluids, such as bronchoalveolar lavage, have improved our understanding of pathobiology of ARDS...
2016: Frontiers in Pediatrics
Victor E Laubach, Ashish K Sharma
PURPOSE OF REVIEW: Lungs are extremely susceptible to injury, and despite advances in surgical management and immunosuppression, outcomes for lung transplantation are the worst of any solid organ transplant. The success of lung transplantation is limited by high rates of primary graft dysfunction because of ischemia-reperfusion injury characterized by robust inflammation, alveolar damage, and vascular permeability. This review will summarize major mechanisms of lung ischemia-reperfusion injury with a focus on the most recent findings in this area...
June 2016: Current Opinion in Organ Transplantation
Alexander Lukasz, Jan Beneke, Kristina Thamm, Jan T Kielstein, Jan Menne, Jan-Henrik Mikesch, Bernhard M W Schmidt, Hermann Haller, Philipp Kümpers, Sascha David, Mario Schiffer
Escherichia coli O104:H4-associated hemolytic uremic syndrome (HUS) is characterized by Shiga toxin-induced vascular damage. As indicated by recent studies, dysregulation of the angiopoietin (Angpt)/Tie2 ligand receptor system may be crucial for endothelial dysfunction in HUS. Early Angpt-2 levels quantified in 48 adult HUS patients were predictive for a complicated clinical course, in particular for need of hemodialysis and mechanical ventilation as well as occurrence of seizures. In vitro challenge of human umbilical vein endothelial cells with patients' sera indicated an injurious mediator role of Angpt-2 opening future perspectives for mitigating endothelial activation in HUS...
2015: Mediators of Inflammation
Raquel S Santos, Lillian Moraes, Cynthia S Samary, Cíntia L Santos, Maíra B A Ramos, Ana P Vasconcellos, Lucas F Horta, Marcelo M Morales, Vera L Capelozzi, Cristiane S N B Garcia, John J Marini, Marcelo Gama de Abreu, Paolo Pelosi, Pedro L Silva, Patricia R M Rocco
BACKGROUND: Large tidal volume (VT) breaths or "recruitment maneuvers" (RMs) are used commonly to open collapsed lungs, but their effectiveness may depend on how the RM is delivered. We hypothesized that a stepped approach to RM delivery ("slow" RM) compared with a nonstepped ("fast" RM), when followed by decremental positive end-expiratory pressure (PEEP) titration to lowest dynamic elastance, would (1) yield a more homogeneous inflation of the lungs, thus reducing the PEEP obtained during post-RM titration; (2) produce less lung morphofunctional injury, regardless of the severity of sepsis-induced acute lung inflammation; and (3) result in less biological damage in severe, but not in moderate, acute lung inflammation...
April 2016: Anesthesia and Analgesia
Pedro Leme Silva, Daniela Negrini, Patricia Rieken Macêdo Rocco
Mechanical ventilation is an essential method of patient support, but it may induce lung damage, leading to ventilator-induced lung injury (VILI). VILI is the result of a complex interplay among various mechanical forces that act on lung structures, such as type I and II epithelial cells, endothelial cells, macrophages, peripheral airways, and the extracellular matrix (ECM), during mechanical ventilation. This article discusses ongoing research focusing on mechanisms of VILI in previously healthy lungs, such as in the perioperative period, and the development of new ventilator strategies for surgical patients...
September 2015: Best Practice & Research. Clinical Anaesthesiology
Li-Fu Li, Chung-Shu Lee, Yung-Yang Liu, Chih-Hao Chang, Chang-Wei Lin, Li-Chung Chiu, Kuo-Chin Kao, Ning-Hung Chen, Cheng-Ta Yang
BACKGROUND: Mechanical ventilation and concomitant administration of hyperoxia in patients with acute respiratory distress syndrome can damage the alveolar epithelial and capillary endothelial barrier by producing inflammatory cytokines and reactive oxygen species. The Src tyrosine kinase and Smad3 are crucial inflammatory regulators used for ventilator-induced lung injury (VILI). The mechanisms regulating interactions between high-tidal-volume mechanical ventilation, hyperoxia, and acute lung injury (ALI) are unclear...
September 16, 2015: Respiratory Research
Nuria E Cabrera-Benítez, Francisco Valladares, Sonia García-Hernández, Ángela Ramos-Nuez, José L Martín-Barrasa, María-Teresa Martínez-Saavedra, Carlos Rodríguez-Gallego, Mercedes Muros, Carlos Flores, Mingyao Liu, Arthur S Slutsky, Jesús Villar
OBJECTIVES: Pulmonary endothelial cell injury is central to the pathophysiology of acute lung injury. Mechanical ventilation can cause endothelial disruption and injury, even in the absence of preexisting inflammation. Platelet-endothelial cell adhesion molecule-1 is a transmembrane protein connecting adjacent endothelial cells. We hypothesized that injurious mechanical ventilation will increase circulating lung endothelial-derived microparticles, defined as microparticles positive for platelet-endothelial cell adhesion molecule-1, which could serve as potential biomarkers and mediators of ventilator-induced lung injury...
December 2015: Critical Care Medicine
Jens Lohser, Peter Slinger
Lung injury is the leading cause of death after thoracic surgery. Initially recognized after pneumonectomy, it has since been described after any period of 1-lung ventilation (OLV), even in the absence of lung resection. Overhydration and high tidal volumes were thought to be responsible at various points; however, it is now recognized that the pathophysiology is more complex and multifactorial. All causative mechanisms known to trigger ventilator-induced lung injury have been described in the OLV setting. The ventilated lung is exposed to high strain secondary to large, nonphysiologic tidal volumes and loss of the normal functional residual capacity...
August 2015: Anesthesia and Analgesia
Wen-Wen Dong, Yu-Jian Liu, Zhou Lv, Yan-Fei Mao, Ying-Wei Wang, Xiao-Yan Zhu, Lai Jiang
High-mobility group box 1 (HMGB1) contributes to lung vascular hyperpermeability during ventilator-induced lung injury. We aimed to determine whether the natural antioxidant resveratrol protected against HMGB1-induced endothelial hyperpermeability both in vitro and in vivo. We found that HMGB1 decreased vascular endothelial (VE)-cadherin expression and increased endothelial permeability, leading to mitochondrial oxidative damage in primary cultured mouse lung vascular endothelial cells (MLVECs). Both the mitochondrial superoxide dismutase 2 mimetic MnTBAP and resveratrol blocked HMGB1-induced mitochondrial oxidative damage, VE-cadherin downregulation, and endothelial hyperpermeability...
November 2015: Free Radical Biology & Medicine
Mingxin Gao, Baodong Xie, Chengxiong Gu, Haitao Li, Fan Zhang, Yang Yu
Pulmonary dysfunction is one of the most frequent complications associated with cardiopulmonary bypass (CPB). Multiple factors, including the contact of blood with the artificial surface of the CPB circuit, ischemia‑reperfusion and lung ventilator arrest elicit inflammatory reactions, consequently resulting in CPB‑induced lung injury. The proinflammatory cytokine tumor necrosis factor‑α (TNF‑α) has been demonstrated to have a critical role in mediating CPB‑induced pulmonary inflammation. The present review evaluated previous studies and summarized the effects of CPB on TNF‑α level in the serum and lung tissue of patients and animal models of CPB, the underlying mechanism of TNF‑α‑mediated lung injury and the therapeutic strategies for the inhibition of TNF‑α activity and production to attenuate CPB‑induced lung injury...
April 2015: Molecular Medicine Reports
Blair Glasgo, Nikunj Bhatt, Sean Reilly
SESSION TITLE: Critical Care Student/Resident Case Report Posters ISESSION TYPE: Medical Student/Resident Case ReportPRESENTED ON: Tuesday, October 28, 2014 at 01:30 PM - 02:30 PMINTRODUCTION: Dobrava is a hantavirus that causes a severe Hemorrhagic Fever with Renal Syndrome (HFRS) and can be associated with nonspecific CNS manifestations. Posterior Reversible Encephalopathy Syndrome (PRES) is a clinicoradiologic syndrome of headache, confusion, visual changes, and seizure with imaging findings of reversible posterior cerebral edema...
October 1, 2014: Chest
Peter M Spieth, Pedro L Silva, Cristiane S N B Garcia, Debora S Ornellas, Cynthia S Samary, Lillian Moraes, Maira Bentes, Marcelo M Morales, Michael Kasper, Andreas Güldner, Robert Huhle, Thea Koch, Paolo Pelosi, Marcelo Gama de Abreu, Patricia R M Rocco
BACKGROUND: Mechanical ventilation can lead to lung biotrauma when mechanical stress exceeds safety thresholds. The authors investigated whether the duration of mechanical stress, that is, the impact of a stress versus time product (STP), influences biotrauma. The authors hypothesized that higher STP levels are associated with increased inflammation and with alveolar epithelial and endothelial cell injury. METHODS: In 46 rats, Escherichia coli lipopolysaccharide (acute lung inflammation) or saline (control) was administered intratracheally...
January 2015: Anesthesiology
Lillian Moraes, Cíntia Lourenco Santos, Raquel Souza Santos, Fernanda Ferreira Cruz, Felipe Saddy, Marcelo Marcos Morales, Vera Luiza Capelozzi, Pedro Leme Silva, Marcelo Gama de Abreu, Cristiane Sousa Nascimento Baez Garcia, Paolo Pelosi, Patricia Rieken Macedo Rocco
INTRODUCTION: Sigh improves oxygenation and lung mechanics during pressure control ventilation (PCV) and pressure support ventilation (PSV) in patients with acute respiratory distress syndrome. However, so far, no study has evaluated the biological impact of sigh during PCV or PSV on the lung and distal organs in experimental pulmonary (p) and extrapulmonary (exp) mild acute lung injury (ALI). METHODS: In 48 Wistar rats, ALI was induced by Escherichia coli lipopolysaccharide either intratracheally (ALIp) or intraperitoneally (ALIexp)...
2014: Critical Care: the Official Journal of the Critical Care Forum
H Schweisfurth, I Sopivnik, R Moog
Transfusion-related acute lung injury (TRALI) is primarily caused by transfusion of fresh frozen plasma or platelet concentrates and occurs by definition within 6 hours after transfusion with acute shortness of breath, hypoxemia and radiographically detectable bilateral infiltrates of the lung. Mostly leucocyte antibodies in the plasma of the blood donor (immunogenic TRALI) are responsible. Apart from antibodies, other substances such as biologically active lipids, mainly arising from the storage of platelet and red blood cell concentrates, can activate neutrophilic granulocytes and trigger a non-immunogenic TRALI...
September 2014: Pneumologie
Sumegha Mitra, Michael S Wade, Xiaoguang Sun, Nurgul Moldobaeva, Carlos Flores, Shwu-Fan Ma, Wei Zhang, Joe G N Garcia, Jeffrey R Jacobson
RATIONALE: Growth arrest DNA damage inducible alpha (GADD45a) is a stress-induced gene we have shown to participate in the pathophysiology of ventilator-induced lung injury (VILI) via regulation of mechanical stress-induced Akt ubiquitination and phosphorylation. The regulation of GADD45a expression by mechanical stress and its relationship with acute lung injury (ALI) susceptibility and severity, however, remains unknown. OBJECTIVES: We examined mechanical stress-dependent regulatory elements (MSRE) in the GADD45a promoter and the contribution of promoter polymorphisms in GADD45a expression and ALI susceptibility...
2014: PloS One
Christopher Uhlig, Pedro L Silva, Débora Ornellas, Raquel S Santos, Paulo J Miranda, Peter M Spieth, Thomas Kiss, Michael Kasper, Bärbel Wiedemann, Thea Koch, Marcelo M Morales, Paolo Pelosi, Marcelo Gama de Abreu, Patricia Rm Rocco
INTRODUCTION: We investigated the effects of intravenous and intratracheal administration of salbutamol on lung morphology and function, expression of ion channels, aquaporin, and markers of inflammation, apoptosis, and alveolar epithelial/endothelial cell damage in experimental pulmonary (p) and extrapulmonary (exp) mild acute respiratory distress syndrome (ARDS). METHODS: In this prospective randomized controlled experimental study, 56 male Wistar rats were randomly assigned to mild ARDS induced by either intratracheal (n = 28, ARDSp) or intraperitoneal (n = 28, ARDSexp) administration of E...
2014: Respiratory Research
Dan N Predescu, Cristina Bardita, Rajive Tandon, Sanda A Predescu
Abstract Acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) are severe syndromes resulting from the diffuse damage of the pulmonary parenchyma. ALI and ARDS are induced by a plethora of local or systemic insults, leading to the activation of multiple pathways responsible for injury, resolution, and repair or scarring of the lungs. Despite the large efforts aimed at exploring the roles of different pathways in humans and animal models and the great strides made in understanding the pathogenesis of ALI/ARDS, the only viable treatment options are still dependent on ventilator and cardiovascular support...
September 2013: Pulmonary Circulation
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