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Huibin Tang, Joseph B Shrager
Mechanical ventilation (MV) is a life-saving measure for those incapable of adequately ventilating or oxygenating without assistance. Unfortunately, even brief periods of MV result in diaphragm weakness (i.e., "ventilator-induced diaphragm dysfunction" - VIDD) that may render it difficult to wean the ventilator. Prolonged MV is associated with cascading complications and is a strong risk factor for death. Thus, prevention of VIDD may have a dramatic impact on mortality rates. Here, we summarized the current understanding of the pathogenic events underlying VIDD...
May 16, 2018: American Journal of Respiratory Cell and Molecular Biology
Laura P B Elbers, Marije Wijnberge, Joost C M Meijers, Dennis C W Poland, Dees P M Brandjes, Eric Fliers, Victor E A Gerdes
INTRODUCTION: Abnormal coagulation tests have been observed in patients with primary hyperparathyroidism (HPT) suggesting a prothrombotic effect of parathyroid hormone (PTH). Vitamin D deficiency (VIDD) is the most frequent cause of secondary HPT. Aim of our study was to investigate the influence of HPT secondary to moderate-to-severe VIDD and vitamin D replacement on the coagulation and fibrinolysis system. SUBJECTS AND METHODS: Prospective cohort study of patients with vitamin D <25 nmol/L with and without HPT, and a control group of patients on vitamin D suppletion...
February 2018: Endocrine Connections
Ashley J Smuder, Kurt J Sollanek, W Bradley Nelson, Kisuk Min, Erin E Talbert, Andreas N Kavazis, Matthew B Hudson, Marco Sandri, Hazel H Szeto, Scott K Powers
Mechanical ventilation (MV) results in the rapid development of ventilator-induced diaphragm dysfunction (VIDD). While the mechanisms responsible for VIDD are not fully understood, recent data reveal that prolonged MV activates autophagy in the diaphragm, which may occur as a result of increased cellular reactive oxygen species (ROS) production. Therefore, we tested the hypothesis that (1) accelerated autophagy is a key contributor to VIDD; and that (2) oxidative stress is required to increase the expression of autophagy genes in the diaphragm...
February 1, 2018: Free Radical Biology & Medicine
Huibin Tang, Catherine L Kennedy, Myung Lee, Yang Gao, Hui Xia, Francesca Olguin, Danielle A Fraga, Kelsey Ayers, Sehoon Choi, Michael Kim, Amir Tehrani, Yasser A Sowb, Thomas A Rando, Joseph B Shrager
Prolonged use of mechanical ventilation (MV) leads to atrophy and dysfunction of the major inspiratory muscle, the diaphragm, contributing to ventilator dependence. Numerous studies have shown that proteolysis and oxidative stress are among the major effectors of ventilator-induced diaphragm muscle dysfunction (VIDD), but the upstream initiator(s) of this process remain to be elucidated. We report here that periodic diaphragm contraction via phrenic nerve stimulation (PNS) substantially reduces MV-induced proteolytic activity and oxidative stress in the diaphragm...
November 6, 2017: Scientific Reports
Arvind Venkat Namuduri, Gabriel Heras, Jia Mi, Nicola Cacciani, Katarina Hörnaeus, Anne Konzer, Sara Bergström Lind, Lars Larsson, Stefano Gastaldello
The small ubiquitin-like modifier (SUMO) is as a regulator of many cellular functions by reversible conjugation to a broad number of substrates. Under endogenous or exogenous perturbations, the SUMO network becomes a fine sensor of stress conditions by alterations in the expression level of SUMO enzymes and consequently changing the status of SUMOylated proteins. The diaphragm is the major inspiratory muscle, which is continuously active under physiological conditions, but its structure and function is severely affected when passively displaced for long extents during mechanical ventilation (MV)...
June 2017: Molecular & Cellular Proteomics: MCP
Stefan Matecki, Boris Jung, Nathalie Saint, Valerie Scheuermann, Samir Jaber, Alain Lacampagne
Respiratory muscle contractile inactivity during mechanical ventilation (MV) induces diaphragm muscle weakness, a condition referred to as ventilator-induced diaphragmatic dysfunction (VIDD). Although VIDD pathophysiological mechanisms are still not fully understood, it has been recently suggested that remodeling of the sarcoplasmic reticulum (SR) calcium release channel/ryanodine receptors (RyR1) in the diaphragm is a proximal mechanism of VIDD. Here, we used piglets, a large animal model of VIDD that is more relevant to human pathophysiology, to determine whether RyR1 alterations are observed in the presence of diaphragm weakness...
February 2017: Journal of Muscle Research and Cell Motility
Lars Larsson, Oliver Friedrich
Critical care and intensive care units (ICUs) have undergone dramatic changes and improvements in recent years, and critical care is today one of the fastest growing hospital disciplines. Significant improvements in treatments, removal of inefficient and harmful interventions, and introduction of advanced technological support systems have improved survival among critically ill ICU patients. However, the improved survival is associated with an increased number of patients with complications related to modern critical care...
December 6, 2016: Comprehensive Physiology
Hannah Ogilvie, Nicola Cacciani, Hazem Akkad, Lars Larsson
Intensive care unit (ICU) patients are often overtly subjected to mechanical ventilation and immobilization, which leads to impaired limb and respiratory muscle function. The latter, termed ventilator-induced diaphragm dysfunction (VIDD) has recently been related to compromised heat shock protein (Hsp) activation. The administration of a pharmacological drug BGP-15 acting as a Hsp chaperone co-inducer has been found to partially alleviate VIDD in young rats. Considering that the mean age in the ICU is increasing, we aimed to explore whether the beneficial functional effects are also present in old rats...
2016: Frontiers in Physiology
Heba Salah, Meishan Li, Nicola Cacciani, Stefano Gastaldello, Hannah Ogilvie, Hazem Akkad, Arvind Venkat Namuduri, Valeria Morbidoni, Konstantin A Artemenko, Gabor Balogh, Vicente Martinez-Redondo, Paulo Jannig, Yvette Hedström, Barry Dworkin, Jonas Bergquist, Jorge Ruas, Laszlo Vigh, Leonardo Salviati, Lars Larsson
Ventilation-induced diaphragm dysfunction (VIDD) is a marked decline in diaphragm function in response to mechanical ventilation, which has negative consequences for individual patients' quality of life and for the health care system, but specific treatment strategies are still lacking. We used an experimental intensive care unit (ICU) model, allowing time-resolved studies of diaphragm structure and function in response to long-term mechanical ventilation and the effects of a pharmacological intervention (the chaperone co-inducer BGP-15)...
August 3, 2016: Science Translational Medicine
Stefan Matecki, Haikel Dridi, Boris Jung, Nathalie Saint, Steven R Reiken, Valérie Scheuermann, Ségolène Mrozek, Gaetano Santulli, Alisa Umanskaya, Basil J Petrof, Samir Jaber, Andrew R Marks, Alain Lacampagne
Ventilator-induced diaphragmatic dysfunction (VIDD) refers to the diaphragm muscle weakness that occurs following prolonged controlled mechanical ventilation (MV). The presence of VIDD impedes recovery from respiratory failure. However, the pathophysiological mechanisms accounting for VIDD are still not fully understood. Here, we show in human subjects and a mouse model of VIDD that MV is associated with rapid remodeling of the sarcoplasmic reticulum (SR) Ca(2+) release channel/ryanodine receptor (RyR1) in the diaphragm...
August 9, 2016: Proceedings of the National Academy of Sciences of the United States of America
Li-Fu Li, Yuh-Lih Chang, Ning-Hung Chen, Chien-Ying Wang, Gwo-Jyh Chang, Meng-Chih Lin, Chih-Hao Chang, Chung-Chi Huang, Jen-Hua Chuang, Yi-Pin Yang, Shih-Hwa Chiou, Yung-Yang Liu
Mechanical ventilation (MV) with hyperoxia is required for providing life support to patients with acute lung injury (ALI). However, MV may cause diaphragm weakness through muscle injury and atrophy, an effect termed ventilator-induced diaphragm dysfunction (VIDD). Src protein tyrosine kinase and class O of forkhead box 1 (FoxO1) mediate acute inflammatory responses and muscle protein degradation induced by oxidative stress. Induced pluripotent stem cells (iPSCs) have been reported to improve hyperoxia-augmented ALI; however, the mechanisms regulating the interactions among VIDD, hyperoxia, and iPSCs are unclear...
July 2016: Translational Research: the Journal of Laboratory and Clinical Medicine
David Berger, Stefan Bloechlinger, Stephan von Haehling, Wolfram Doehner, Jukka Takala, Werner J Z'Graggen, Joerg C Schefold
Muscular weakness and muscle wasting may often be observed in critically ill patients on intensive care units (ICUs) and may present as failure to wean from mechanical ventilation. Importantly, mounting data demonstrate that mechanical ventilation itself may induce progressive dysfunction of the main respiratory muscle, i.e. the diaphragm. The respective condition was termed 'ventilator-induced diaphragmatic dysfunction' (VIDD) and should be distinguished from peripheral muscular weakness as observed in 'ICU-acquired weakness (ICU-AW)'...
September 2016: Journal of Cachexia, Sarcopenia and Muscle
Won-Young Kim, So Hee Park, Won Young Kim, Jin Won Huh, Sang-Bum Hong, Younsuck Koh, Chae-Man Lim
PURPOSE: To evaluate the effect of theophylline in patients with ventilator-induced diaphragmatic dysfunction (VIDD). MATERIALS AND METHODS: Patients who required mechanical ventilation at least 72 hours, met the criteria for a spontaneous breathing trial, and had evidence of VIDD by ultrasonography were included in the study. RESULTS: Of the 40 patients, 21 received theophylline and 19 did not. Clinical characteristics were similar in the 2 groups...
June 2016: Journal of Critical Care
Tom Schepens, Walter Verbrugghe, Karolien Dams, Bob Corthouts, Paul M Parizel, Philippe G Jorens
INTRODUCTION: Mechanical ventilation and the effect of respiratory muscle unloading on the diaphragm cause ventilator-induced diaphragmatic dysfunction (VIDD). Atrophy of the diaphragmatic muscle is a major part of VIDD, and has a rapid onset in most animal models. We wanted to assess the clinical evolution and risk factors for VIDD in an adult intensive care unit (ICU) by measuring diaphragm thickness using ultrasound. METHOD: We performed a single-centre observational cohort study, including 54 mechanically ventilated patients...
December 7, 2015: Critical Care: the Official Journal of the Critical Care Forum
Basil J Petrof, Sabah N Hussain
PURPOSE OF REVIEW: The purpose of the review is to summarize and discuss recent research regarding the role of mechanical ventilation in producing weakness and atrophy of the diaphragm in critically ill patients, an entity termed ventilator-induced diaphragmatic dysfunction (VIDD). RECENT FINDINGS: Severe weakness of the diaphragm is frequent in mechanically ventilated patients, in whom it contributes to poor outcomes including increased mortality. Significant progress has been made in identifying the molecular mechanisms responsible for VIDD in animal models, and there is accumulating evidence for occurrence of the same cellular processes in the diaphragms of human patients undergoing prolonged mechanical ventilation...
February 2016: Current Opinion in Critical Care
Ashley J Smuder, Elisa J Gonzalez-Rothi, Oh Sung Kwon, Aaron B Morton, Kurt J Sollanek, Scott K Powers, David D Fuller
Cervical spinal cord injury (SCI) can dramatically impair diaphragm muscle function and often necessitates mechanical ventilation (MV) to maintain adequate pulmonary gas exchange. MV is a life-saving intervention. However, prolonged MV results in atrophy and impaired function of the diaphragm. Since cervical SCI can also trigger diaphragm atrophy, it may create preconditions that exacerbate ventilator-induced diaphragm dysfunction (VIDD). Currently, no drug therapy or clinical standard of care exists to prevent or minimize diaphragm dysfunction following SCI...
January 15, 2016: Journal of Applied Physiology
Ilan Azuelos, Boris Jung, Martin Picard, Feng Liang, Tong Li, Christian Lemaire, Christian Giordano, Sabah Hussain, Basil J Petrof
BACKGROUND: Mechanical ventilation (MV) is associated with atrophy and weakness of the diaphragm muscle, a condition termed ventilator-induced diaphragmatic dysfunction (VIDD). Autophagy is a lysosomally mediated proteolytic process that can be activated by oxidative stress, which has the potential to either mitigate or exacerbate VIDD. The primary goals of this study were to (1) determine the effects of MV on autophagy in the diaphragm and (2) evaluate the impact of antioxidant therapy on autophagy induction and MV-induced diaphragmatic weakness...
June 2015: Anesthesiology
Kurt J Sollanek, Ashley J Smuder, Michael P Wiggs, Aaron B Morton, Lauren G Koch, Steven L Britton, Scott K Powers
Prolonged mechanical ventilation (MV) leads to rapid diaphragmatic atrophy and contractile dysfunction, which is collectively termed "ventilator-induced diaphragm dysfunction" (VIDD). Interestingly, endurance exercise training prior to MV has been shown to protect against VIDD. Further, recent evidence reveals that sedentary animals selectively bred to possess a high aerobic capacity possess a similar skeletal muscle phenotype to muscles from endurance trained animals. Therefore, we tested the hypothesis that animals with a high intrinsic aerobic capacity would naturally be afforded protection against VIDD...
April 1, 2015: Journal of Applied Physiology
B Jung, D Gleeton, A Daurat, M Conseil, M Mahul, G Rao, S Matecki, A Lacampagne, S Jaber
INTRODUCTION: Mechanical ventilation is associated with ventilator-induced diaphragmatic dysfunction (VIDD) in animal models and also in humans. BACKGROUND: The main pathophysiological pathways implicated in VIDD seems to be related to muscle inactivity but may also be the consequence of high tidal volumes. Systemic insults from side effects of medication, infection, malnutrition and hypoperfusion also play a part. The diaphragm is caught in the cross-fire of ventilation-induced and systemic-induced dysfunctions...
April 2015: Revue des Maladies Respiratoires
Huibin Tang, Ira J Smith, Sabah N A Hussain, Peter Goldberg, Myung Lee, Sista Sugiarto, Guillermo L Godinez, Baljit K Singh, Donald G Payan, Thomas A Rando, Todd M Kinsella, Joseph B Shrager
Mechanical ventilation (MV) is one of the lynchpins of modern intensive-care medicine and is life saving in many critically ill patients. Continuous ventilator support, however, results in ventilation-induced diaphragm dysfunction (VIDD) that likely prolongs patients' need for MV and thereby leads to major associated complications and avoidable intensive care unit (ICU) deaths. Oxidative stress is a key pathogenic event in the development of VIDD, but its regulation remains largely undefined. We report here that the JAK-STAT pathway is activated in MV in the human diaphragm, as evidenced by significantly increased phosphorylation of JAK and STAT...
2014: Molecular Medicine
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