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  1. Article ; Online: Acute procedural efficacy and safety of a novel cryoballoon for the treatment of paroxysmal atrial fibrillation: Results from the POLAR ICE study.

    Martin, Claire A / Tilz, Roland R R / Anic, Ante / Defaye, Pascal / Luik, Armin / de Asmundis, Carlo / Champ-Rigot, Laure / Iacopino, Saverio / Sommer, Philipp / Albrecht, Elizabeth M / Raybuck, Jonathan D / Richards, Elizabeth / Cielen, Nele / Yap, Sing-Chien

    Journal of cardiovascular electrophysiology

    2023  Volume 34, Issue 4, Page(s) 833–840

    Abstract: Introduction: Pulmonary vein isolation (PVI) is well established as a primary treatment for atrial fibrillation (AF). The POLAR ICE study was designed to collect prospective real world data on the safety and effectiveness of the POLARx: Methods: ... ...

    Abstract Introduction: Pulmonary vein isolation (PVI) is well established as a primary treatment for atrial fibrillation (AF). The POLAR ICE study was designed to collect prospective real world data on the safety and effectiveness of the POLARx
    Methods: POLAR ICE, a prospective, non-randomized, multicenter (international) registry (NCT04250714), enrolled 399 patients across 19 European centers. Procedural characteristics, such as time to isolation, cryoablations per pulmonary vein (PV), balloon nadir temperature, and occlusion grade were recorded. PVI was confirmed with entrance block testing.
    Results: Data on 372 de novo PVI procedures (n = 2190 ablations) were collected. Complete PVI was achieved in 96.8% of PVs. Procedure and fluoroscopy times were 68.2 ± 24.6 and 15.6 ± 9.6 min, respectively. Left atrial dwell time was 46.6 ± 18.3 min. Grade 3 or 4 occlusion was achieved in 98.2% of PVs reported and 71.2% of PVs isolation required only a single cryoablation. Of 2190 cryoapplications, 83% had a duration of at least 120 s; nadir temperature of these ablations averaged -56.3 ± 6.5°C. There were 6 phrenic nerve palsy events, 2 of which resolved within 3 months of the procedure.
    Conclusion: This real-world usage data on a novel cryoballoon suggests this device is effective, safe, and relatively fast in centers with cryoballoon experience. These data are comparable to prior POLARx reports and in keeping with reported data on other cryoballoons. Future studies should examine the long-term outcomes and the relationship between biophysical parameters and outcomes for this novel cryoballoon.
    MeSH term(s) Humans ; Atrial Fibrillation/surgery ; Prospective Studies ; Treatment Outcome ; Heart Atria ; Fluoroscopy
    Language English
    Publishing date 2023-02-23
    Publishing country United States
    Document type Multicenter Study ; Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 1025989-2
    ISSN 1540-8167 ; 1045-3873
    ISSN (online) 1540-8167
    ISSN 1045-3873
    DOI 10.1111/jce.15861
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  2. Article ; Online: Novel cryoballoon to isolate pulmonary veins in patients with paroxysmal atrial fibrillation: long-term outcomes in a multicentre clinical study.

    Martin, Andrew / Fowler, Marina / Breskovic, Toni / Ouss, Alexandre / Dekker, Lukas / Yap, Sing-Chien / Bhagwandien, Rohit / Albrecht, Elizabeth M / Cielen, Nele / Richards, Elizabeth / Tran, Binh C / Lever, Nigel / Anic, Ante

    Journal of interventional cardiac electrophysiology : an international journal of arrhythmias and pacing

    2022  Volume 65, Issue 3, Page(s) 609–616

    Abstract: Background: Recently, a novel cryoballoon ablation catheter has demonstrated acute safety and efficacy in de novo pulmonary vein isolation (PVI) procedures in patients with paroxysmal atrial fibrillation (PAF). However, there are limited studies ... ...

    Abstract Background: Recently, a novel cryoballoon ablation catheter has demonstrated acute safety and efficacy in de novo pulmonary vein isolation (PVI) procedures in patients with paroxysmal atrial fibrillation (PAF). However, there are limited studies demonstrating the long-term efficacy. The aim of this study was to evaluate the long-term safety and efficacy of this novel cryoballoon in treating PAF.
    Methods: This was a non-randomized, prospective, multicentre study enrolling 58 consecutive patients. Cryoablation was delivered for 180 s if time to isolation was ≤ 60 s. Otherwise a 240-s cryoablation was performed. One centre performed pre- and post-ablation high-density mapping (n = 9) to characterize lesion formation. After a 3-month blanking period, recurrence was defined as having any documented, symptomatic episode(s) of AF or atrial tachycardia. All patients were followed for 1 year.
    Results: Acute PVI was achieved in 230 of 231 pulmonary veins (99.6%) with 5.3 ± 1.6 cryoablations per patient (1.3 ± 0.7 cryoablations per vein). Forty-three (77%) patients remained arrhythmia-free at 1-year follow-up. Four patients (6.9%) experienced phrenic nerve injury (3 resolved during the index procedure; 1 resolved at 6 months). One serious adverse device event was reported: femoral arterial embolism event occurring 2 weeks post-index procedure. For patients who underwent high-density mapping, cryoablation was antral with 50% of the posterior wall ablated.
    Conclusions: Initial multicentre clinical experience with a novel cryoballoon has demonstrated safety and efficacy of PVI in patients with PAF. Ablation with this cryoballoon provides a wide, antral lesion set with significant debulking of the posterior wall of the left atrium.
    MeSH term(s) Humans ; Pulmonary Veins/surgery ; Atrial Fibrillation/surgery ; Prospective Studies
    Language English
    Publishing date 2022-04-12
    Publishing country Netherlands
    Document type Multicenter Study ; Journal Article
    ZDB-ID 1329179-8
    ISSN 1572-8595 ; 1383-875X
    ISSN (online) 1572-8595
    ISSN 1383-875X
    DOI 10.1007/s10840-022-01200-5
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  3. Article ; Online: Musculoskeletal disorders in chronic obstructive pulmonary disease.

    Cielen, Nele / Maes, Karen / Gayan-Ramirez, Ghislaine

    BioMed research international

    2014  Volume 2014, Page(s) 965764

    Abstract: Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by airway obstruction and inflammation but also accompanied by several extrapulmonary consequences, such as skeletal muscle weakness and osteoporosis. Skeletal muscle weakness ... ...

    Abstract Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by airway obstruction and inflammation but also accompanied by several extrapulmonary consequences, such as skeletal muscle weakness and osteoporosis. Skeletal muscle weakness is of major concern, since it leads to poor functional capacity, impaired health status, increased healthcare utilization, and even mortality, independently of lung function. Osteoporosis leads to fractures and is associated with increased mortality, functional decline, loss of quality of life, and need for institutionalization. Therefore, the presence of the combination of these comorbidities will have a negative impact on daily life in patients with COPD. In this review, we will focus on these two comorbidities, their prevalence in COPD, combined risk factors, and pathogenesis. We will try to prove the clustering of these comorbidities and discuss possible preventive or therapeutic strategies.
    MeSH term(s) Health Status ; Humans ; Musculoskeletal Diseases/etiology ; Musculoskeletal Diseases/mortality ; Musculoskeletal Diseases/therapy ; Prevalence ; Pulmonary Disease, Chronic Obstructive/complications ; Pulmonary Disease, Chronic Obstructive/mortality ; Pulmonary Disease, Chronic Obstructive/therapy ; Quality of Life
    Language English
    Publishing date 2014-03-25
    Publishing country United States
    Document type Journal Article ; Review
    ZDB-ID 2698540-8
    ISSN 2314-6141 ; 2314-6133
    ISSN (online) 2314-6141
    ISSN 2314-6133
    DOI 10.1155/2014/965764
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  4. Article ; Online: Musculoskeletal Disorders in Chronic Obstructive Pulmonary Disease

    Nele Cielen / Karen Maes / Ghislaine Gayan-Ramirez

    BioMed Research International, Vol

    2014  Volume 2014

    Abstract: Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by airway obstruction and inflammation but also accompanied by several extrapulmonary consequences, such as skeletal muscle weakness and osteoporosis. Skeletal muscle weakness ... ...

    Abstract Chronic obstructive pulmonary disease (COPD) is a lung disease characterized by airway obstruction and inflammation but also accompanied by several extrapulmonary consequences, such as skeletal muscle weakness and osteoporosis. Skeletal muscle weakness is of major concern, since it leads to poor functional capacity, impaired health status, increased healthcare utilization, and even mortality, independently of lung function. Osteoporosis leads to fractures and is associated with increased mortality, functional decline, loss of quality of life, and need for institutionalization. Therefore, the presence of the combination of these comorbidities will have a negative impact on daily life in patients with COPD. In this review, we will focus on these two comorbidities, their prevalence in COPD, combined risk factors, and pathogenesis. We will try to prove the clustering of these comorbidities and discuss possible preventive or therapeutic strategies.
    Keywords Medicine ; R
    Subject code 610
    Language English
    Publishing date 2014-01-01T00:00:00Z
    Publisher Hindawi Limited
    Document type Article ; Online
    Database BASE - Bielefeld Academic Search Engine (life sciences selection)

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  5. Article ; Online: The effects of smoking on whisker movements: A quantitative measure of exploratory behaviour in rodents.

    Grant, Robyn A / Cielen, Nele / Maes, Karen / Heulens, Nele / Galli, Gina L J / Janssens, Wim / Gayan-Ramirez, Ghislaine / Degens, Hans

    Behavioural processes

    2016  Volume 128, Page(s) 17–23

    Abstract: Nicotine, an important component of cigarette smoke, is a neurotransmitter that contributes to stress, depression and anxiety in smokers. In rodents, it increases anxiety and reduces exploratory behaviours. However, so far, the measurements of ... ...

    Abstract Nicotine, an important component of cigarette smoke, is a neurotransmitter that contributes to stress, depression and anxiety in smokers. In rodents, it increases anxiety and reduces exploratory behaviours. However, so far, the measurements of exploratory behaviour in rodents have only been semi-quantitative and lacking in sufficient detail to characterise the temporal effect of smoking cessation. As rodents, such as mice and rats, primarily use whiskers to explore their environment, we studied the effect of 3 months smoking with 1 and 2 weeks smoking cessation on whisker movements in mice, using high-speed video camera footage and image analysis. Both protraction and retraction whisker velocities were increased in smoking mice (p<0.001) and returned to normal following just one week of smoking cessation. In addition, locomotion speeds were decreased in smoking mice, and returned to normal following smoking cessation. Lung function was also impacted by smoking and remained impaired even following smoking cessation. We suggest that the increased whisker velocities in the smoking mice reflect reduced exploration and impeded tactile performance. The increase in whisker velocity with smoking, and its reduction following smoking cessation, also lends support to acetylcholine being involved in awareness, attention and alertness pathways. It also shows that smoking-induced behavioural changes can be reversed with smoking cessation, which may have implications for human smokers.
    MeSH term(s) Animals ; Exploratory Behavior/drug effects ; Locomotion/drug effects ; Lung Compliance/drug effects ; Male ; Mice ; Smoking/adverse effects ; Smoking Cessation ; Vibrissae/drug effects ; Vibrissae/physiology ; Video Recording
    Language English
    Publishing date 2016-07
    Publishing country Netherlands
    Document type Journal Article
    ZDB-ID 196999-7
    ISSN 1872-8308 ; 0376-6357
    ISSN (online) 1872-8308
    ISSN 0376-6357
    DOI 10.1016/j.beproc.2016.03.021
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  6. Article ; Online: Interaction between Physical Activity and Smoking on Lung, Muscle, and Bone in Mice.

    Cielen, Nele / Maes, Karen / Heulens, Nele / Troosters, Thierry / Carmeliet, Geert / Janssens, Wim / Gayan-Ramirez, Ghislaine N

    American journal of respiratory cell and molecular biology

    2016  Volume 54, Issue 5, Page(s) 674–682

    Abstract: Physical inactivity is an important contributor to skeletal muscle weakness, osteoporosis, and weight loss in chronic obstructive pulmonary disease. However, the effects of physical inactivity, in interaction with smoking, on lung, muscle, and bone are ... ...

    Abstract Physical inactivity is an important contributor to skeletal muscle weakness, osteoporosis, and weight loss in chronic obstructive pulmonary disease. However, the effects of physical inactivity, in interaction with smoking, on lung, muscle, and bone are poorly understood. To address this issue, male mice were randomly assigned to an active (daily running), moderately inactive (space restriction), or extremely inactive group (space restriction followed by hindlimb suspension to mimic bed rest) during 24 weeks and simultaneously exposed to either cigarette smoke or room air. The effects of different physical activity levels and smoking status and their respective interaction were examined on lung function, body composition, in vitro limb muscle function, and bone parameters. Smoking caused emphysema, reduced food intake with subsequent loss of body weight, and fat, lean, and muscle mass, but increased trabecular bone volume. Smoking induced muscle fiber atrophy, which did not result in force impairment. Moderate inactivity only affected lung volumes and compliance, whereas extreme inactivity increased lung inflammation, lowered body and fat mass, induced fiber atrophy with soleus muscle dysfunction, and reduced exercise capacity and all bone parameters. When combined with smoking, extreme inactivity also aggravated lung inflammation and emphysema, and accelerated body and muscle weight loss. This study shows that extreme inactivity, especially when imposed by absolute rest, accelerates lung damage and inflammation. When combined with smoking, extreme inactivity is deleterious for muscle bulk, bone, and lungs. These data highlight that the consequences of physical inactivity during the course of chronic obstructive pulmonary disease should not be neglected.
    MeSH term(s) Animals ; Body Composition ; Body Weight ; Bone and Bones/physiopathology ; Cell Count ; Feeding Behavior ; Lung/pathology ; Lung/physiopathology ; Male ; Mice, Inbred C57BL ; Muscle, Skeletal/physiopathology ; Neutrophils/pathology ; Organ Size ; Physical Conditioning, Animal ; Pneumonia/pathology ; Respiratory Function Tests ; Smoking/adverse effects
    Language English
    Publishing date 2016-05
    Publishing country United States
    Document type Journal Article
    ZDB-ID 1025960-0
    ISSN 1535-4989 ; 1044-1549
    ISSN (online) 1535-4989
    ISSN 1044-1549
    DOI 10.1165/rcmb.2015-0181OC
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  7. Article ; Online: Vitamin D deficiency impairs skeletal muscle function in a smoking mouse model.

    Cielen, Nele / Heulens, Nele / Maes, Karen / Carmeliet, Geert / Mathieu, Chantal / Janssens, Wim / Gayan-Ramirez, Ghislaine

    The Journal of endocrinology

    2016  Volume 229, Issue 2, Page(s) 97–108

    Abstract: Chronic obstructive pulmonary disease (COPD) is associated with skeletal muscle dysfunction. Vitamin D plays an important role in muscle strength and performance in healthy individuals. Vitamin D deficiency is highly prevalent in COPD, but its role in ... ...

    Abstract Chronic obstructive pulmonary disease (COPD) is associated with skeletal muscle dysfunction. Vitamin D plays an important role in muscle strength and performance in healthy individuals. Vitamin D deficiency is highly prevalent in COPD, but its role in skeletal muscle dysfunction remains unclear. We examined the time-course effect of vitamin D deficiency on limb muscle function in mice with normal or deficient vitamin D serum levels exposed to air or cigarette smoke for 6, 12 or 18 weeks. The synergy of smoking and vitamin D deficiency increased lung inflammation and lung compliance from 6 weeks on with highest emphysema scores observed at 18 weeks. Smoking reduced body and muscle mass of the soleus and extensor digitorum longus (EDL), but did not affect contractility, despite type II atrophy. Vitamin D deficiency did not alter muscle mass but reduced muscle force over time, downregulated vitamin D receptor expression, and increased muscle lipid peroxidation but did not alter actin and myosin expression, fiber dimensions or twitch relaxation time. The combined effect of smoking and vitamin D deficiency did not further deteriorate muscle function but worsened soleus mass loss and EDL fiber atrophy at 18 weeks. We conclude that the synergy of smoking and vitamin D deficiency in contrast to its effect on lung disease, had different, independent but important noxious effects on skeletal muscles in a mouse model of mild COPD.
    MeSH term(s) Actins/metabolism ; Animals ; Disease Models, Animal ; Male ; Mice ; Mice, Inbred C57BL ; Muscle Contraction ; Muscle, Skeletal/pathology ; Muscle, Skeletal/physiopathology ; Myosins/metabolism ; Oxidative Stress ; Pulmonary Disease, Chronic Obstructive/complications ; Pulmonary Disease, Chronic Obstructive/pathology ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Receptors, Calcitriol/metabolism ; Smoking/adverse effects ; Smoking/pathology ; Smoking/physiopathology ; Vitamin D/analogs & derivatives ; Vitamin D/blood ; Vitamin D Deficiency/complications ; Vitamin D Deficiency/pathology ; Vitamin D Deficiency/physiopathology
    Chemical Substances Actins ; Receptors, Calcitriol ; Vitamin D (1406-16-2) ; 25-hydroxyvitamin D (A288AR3C9H) ; Myosins (EC 3.6.4.1)
    Language English
    Publishing date 2016
    Publishing country England
    Document type Journal Article
    ZDB-ID 3028-4
    ISSN 1479-6805 ; 0022-0795
    ISSN (online) 1479-6805
    ISSN 0022-0795
    DOI 10.1530/JOE-15-0491
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  8. Article: The effects of smoking on whisker movements: A quantitative measure of exploratory behaviour in rodents

    Grant, Robyn A / Ghislaine Gayan-Ramirez / Gina L.J. Galli / Hans Degens / Karen Maes / Nele Cielen / Nele Heulens / Wim Janssens

    Behavioural processes. 2016 July, v. 128

    2016  

    Abstract: Nicotine, an important component of cigarette smoke, is a neurotransmitter that contributes to stress, depression and anxiety in smokers. In rodents, it increases anxiety and reduces exploratory behaviours. However, so far, the measurements of ... ...

    Abstract Nicotine, an important component of cigarette smoke, is a neurotransmitter that contributes to stress, depression and anxiety in smokers. In rodents, it increases anxiety and reduces exploratory behaviours. However, so far, the measurements of exploratory behaviour in rodents have only been semi-quantitative and lacking in sufficient detail to characterise the temporal effect of smoking cessation. As rodents, such as mice and rats, primarily use whiskers to explore their environment, we studied the effect of 3 months smoking with 1 and 2 weeks smoking cessation on whisker movements in mice, using high-speed video camera footage and image analysis. Both protraction and retraction whisker velocities were increased in smoking mice (p<0.001) and returned to normal following just one week of smoking cessation. In addition, locomotion speeds were decreased in smoking mice, and returned to normal following smoking cessation. Lung function was also impacted by smoking and remained impaired even following smoking cessation. We suggest that the increased whisker velocities in the smoking mice reflect reduced exploration and impeded tactile performance. The increase in whisker velocity with smoking, and its reduction following smoking cessation, also lends support to acetylcholine being involved in awareness, attention and alertness pathways. It also shows that smoking-induced behavioural changes can be reversed with smoking cessation, which may have implications for human smokers.
    Keywords acetylcholine ; anxiety ; behavior change ; cigarettes ; humans ; image analysis ; locomotion ; lung function ; mice ; neurotransmitters ; nicotine ; rats ; video cameras
    Language English
    Dates of publication 2016-07
    Size p. 17-23.
    Publishing place Elsevier B.V.
    Document type Article
    ZDB-ID 196999-7
    ISSN 1872-8308 ; 0376-6357
    ISSN (online) 1872-8308
    ISSN 0376-6357
    DOI 10.1016/j.beproc.2016.03.021
    Database NAL-Catalogue (AGRICOLA)

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  9. Article ; Online: Vitamin D deficiency exacerbates COPD-like characteristics in the lungs of cigarette smoke-exposed mice.

    Heulens, Nele / Korf, Hannelie / Cielen, Nele / De Smidt, Elien / Maes, Karen / Gysemans, Conny / Verbeken, Erik / Gayan-Ramirez, Ghislaine / Mathieu, Chantal / Janssens, Wim

    Respiratory research

    2015  Volume 16, Page(s) 110

    Abstract: Background: Chronic obstructive pulmonary disease (COPD) is characterized by excessive inflammation and disturbed bacterial clearance in the airways. Although cigarette smoke (CS) exposure poses a major risk, vitamin D deficiency could potentially ... ...

    Abstract Background: Chronic obstructive pulmonary disease (COPD) is characterized by excessive inflammation and disturbed bacterial clearance in the airways. Although cigarette smoke (CS) exposure poses a major risk, vitamin D deficiency could potentially contribute to COPD progression. Many in vitro studies demonstrate important anti-inflammatory and antibacterial effects of vitamin D, but a direct contribution of vitamin D deficiency to COPD onset and disease progression has not been explored.
    Methods: In the current study, we used a murine experimental model to investigate the combined effect of vitamin D deficiency and CS exposure on the development of COPD-like characteristics. Therefore, vitamin D deficient or control mice were exposed to CS or ambient air for a period of 6 (subacute) or 12 weeks (chronic). Besides lung function and structure measurements, we performed an in depth analysis of the size and composition of the cellular infiltrate in the airways and lung parenchyma and tested the ex vivo phagocytic and oxidative burst capacity of alveolar macrophages.
    Results: Vitamin D deficient mice exhibited an accelerated lung function decline following CS exposure compared to control mice. Furthermore, early signs of emphysema were only observed in CS-exposed vitamin D deficient mice, which was accompanied by elevated levels of MMP-12 in the lung. Vitamin D deficient mice showed exacerbated infiltration of inflammatory cells in the airways and lung parenchyma after both subacute and chronic CS exposure compared to control mice. Furthermore, elevated levels of typical proinflammatory cytokines and chemokines could be detected in the bronchoalveolar lavage fluid (KC and TNF-α) and lung tissue (IP-10, MCP-1, IL-12) of CS-exposed vitamin D deficient mice compared to control mice. Finally, although CS greatly impaired the ex vivo phagocytic and oxidative burst function of alveolar macrophages, vitamin D deficient mice did not feature an additional defect.
    Conclusions: Our data demonstrate that vitamin D deficiency both accelerates and aggravates the development of characteristic disease features of COPD. As vitamin D deficiency is highly prevalent, large randomized trials exploring effects of vitamin D supplementation on lung function decline and COPD onset are needed.
    MeSH term(s) Animals ; Bronchoalveolar Lavage Fluid/chemistry ; Calcium/blood ; Cytokines/metabolism ; Disease Models, Animal ; Disease Progression ; Female ; Inflammation Mediators/metabolism ; Lung/metabolism ; Lung/pathology ; Lung/physiopathology ; Macrophage Activation ; Macrophages, Alveolar ; Male ; Matrix Metalloproteinase 12/metabolism ; Mice, Inbred C57BL ; Phagocytosis ; Pneumonia/etiology ; Pneumonia/physiopathology ; Pulmonary Disease, Chronic Obstructive/diagnosis ; Pulmonary Disease, Chronic Obstructive/etiology ; Pulmonary Disease, Chronic Obstructive/metabolism ; Pulmonary Disease, Chronic Obstructive/physiopathology ; Pulmonary Emphysema/etiology ; Pulmonary Emphysema/physiopathology ; Respiratory Burst ; Risk Factors ; Smoke ; Smoking/adverse effects ; Time Factors ; Vitamin D/analogs & derivatives ; Vitamin D/blood ; Vitamin D Deficiency/complications ; Vitamin D Deficiency/diagnosis ; Vitamin D Deficiency/metabolism
    Chemical Substances Cytokines ; Inflammation Mediators ; Smoke ; Vitamin D (1406-16-2) ; 25-hydroxyvitamin D (A288AR3C9H) ; Matrix Metalloproteinase 12 (EC 3.4.24.65) ; matrix metallopeptidase 12, mouse (EC 3.4.24.65) ; Calcium (SY7Q814VUP)
    Language English
    Publishing date 2015-09-16
    Publishing country England
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 2041675-1
    ISSN 1465-993X ; 1465-9921
    ISSN (online) 1465-993X
    ISSN 1465-9921
    DOI 10.1186/s12931-015-0271-x
    Database MEDical Literature Analysis and Retrieval System OnLINE

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  10. Article ; Online: Sedation using propofol induces similar diaphragm dysfunction and atrophy during spontaneous breathing and mechanical ventilation in rats.

    Bruells, Christian S / Maes, Karen / Rossaint, Rolf / Thomas, Debby / Cielen, Nele / Bergs, Ingmar / Bleilevens, Christian / Weis, Joachim / Gayan-Ramirez, Ghislaine

    Anesthesiology

    2014  Volume 120, Issue 3, Page(s) 665–672

    Abstract: Background: Mechanical ventilation is crucial for patients with respiratory failure. The mechanical takeover of diaphragm function leads to diaphragm dysfunction and atrophy (ventilator-induced diaphragmatic dysfunction), with an increase in oxidative ... ...

    Abstract Background: Mechanical ventilation is crucial for patients with respiratory failure. The mechanical takeover of diaphragm function leads to diaphragm dysfunction and atrophy (ventilator-induced diaphragmatic dysfunction), with an increase in oxidative stress as a major contributor. In most patients, a sedative regimen has to be initiated to allow tube tolerance and ventilator synchrony. Clinical data imply a correlation between cumulative propofol dosage and diaphragm dysfunction, whereas laboratory investigations have revealed that propofol has some antioxidant properties. The authors hypothesized that propofol reduces markers of oxidative stress, atrophy, and contractile dysfunction in the diaphragm.
    Methods: Male Wistar rats (n = 8 per group) were subjected to either 24 h of mechanical ventilation or were undergone breathing spontaneously for 24 h under propofol sedation to test for drug effects. Another acutely sacrificed group served as controls. After sacrifice, diaphragm tissue was removed, and contractile properties, cross-sectional areas, oxidative stress, and proteolysis were examined. The gastrocnemius served as internal control.
    Results: Propofol did not protect against diaphragm atrophy, oxidative stress, and protease activation. The decrease in tetanic force compared with controls was similar in the spontaneous breathing group (31%) and in the ventilated group (34%), and both groups showed the same amount of muscle atrophy. The gastrocnemius muscle fibers did not show atrophy.
    Conclusions: Propofol does not protect against ventilator-induced diaphragmatic dysfunction or oxidative injury. Notably, spontaneous breathing under propofol sedation resulted in the same amount of diaphragm atrophy and dysfunction although diaphragm activation per se protects against ventilator-induced diaphragmatic dysfunction. This makes a drug effect of propofol likely.
    MeSH term(s) Analysis of Variance ; Anesthetics, Intravenous/pharmacology ; Animals ; Diaphragm/drug effects ; Diaphragm/physiopathology ; Disease Models, Animal ; Male ; Muscular Atrophy/physiopathology ; Oxidative Stress/drug effects ; Propofol/pharmacology ; Rats ; Rats, Wistar ; Respiration ; Respiration, Artificial/methods ; Ventilator-Induced Lung Injury/physiopathology
    Chemical Substances Anesthetics, Intravenous ; Propofol (YI7VU623SF)
    Language English
    Publishing date 2014-03
    Publishing country United States
    Document type Journal Article ; Research Support, Non-U.S. Gov't
    ZDB-ID 269-0
    ISSN 1528-1175 ; 0003-3022
    ISSN (online) 1528-1175
    ISSN 0003-3022
    DOI 10.1097/ALN.0000000000000125
    Database MEDical Literature Analysis and Retrieval System OnLINE

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