Mechanical Ventilation

14,000,000 Leading Edge Experts on the ideXlab platform

Scan Science and Technology

Contact Leading Edge Experts & Companies

Scan Science and Technology

Contact Leading Edge Experts & Companies

The Experts below are selected from a list of 175149 Experts worldwide ranked by ideXlab platform

Cheng-ta Yang - One of the best experts on this subject based on the ideXlab platform.

  • lumican expression in diaphragm induced by Mechanical Ventilation
    PLOS ONE, 2011
    Co-Authors: Cheng-ta Yang, Lifu Li, Baoxiang Chen, Yinghuang Tsai
    Abstract:

    Background Diaphragmatic dysfunction found in the patients with acute lung injury required prolonged Mechanical Ventilation. Mechanical Ventilation can induce production of inflammatory cytokines and excess deposition of extracellular matrix proteins via up-regulation of transforming growth factor (TGF)-β1. Lumican is known to participate in TGF-β1 signaling during wound healing. The mechanisms regulating interactions between Mechanical Ventilation and diaphragmatic injury are unclear. We hypothesized that diaphragmatic damage by short duration of Mechanical stretch caused up-regulation of lumican that modulated TGF-β1 signaling. Methods Male C57BL/6 mice, either wild-type or lumican-null, aged 3 months, weighing between 25 and 30 g, were exposed to normal tidal volume (10 ml/kg) or high tidal volume (30 ml/kg) Mechanical Ventilation with room air for 2 to 8 hours. Nonventilated mice served as control groups. Results High tidal volume Mechanical Ventilation induced interfibrillar disassembly of diaphragmatic collagen fiber, lumican activation, type I and III procollagen, fibronectin, and α-smooth muscle actin (α-SMA) mRNA, production of free radical and TGF-β1 protein, and positive staining of lumican in diaphragmatic fiber. Mechanical Ventilation of lumican deficient mice attenuated diaphragmatic injury, type I and III procollagen, fibronectin, and α-SMA mRNA, and production of free radical and TGF-β1 protein. No significant diaphragmatic injury was found in mice subjected to normal tidal volume Mechanical Ventilation. Conclusion Our data showed that high tidal volume Mechanical Ventilation induced TGF-β1 production, TGF-β1-inducible genes, e.g., collagen, and diaphragmatic dysfunction through activation of the lumican.

Scott K Powers - One of the best experts on this subject based on the ideXlab platform.

  • trolox attenuates Mechanical Ventilation induced diaphragmatic dysfunction and proteolysis
    American Journal of Respiratory and Critical Care Medicine, 2004
    Co-Authors: Jenna L Betters, David S Criswell, Andrew R Shanely, Darin Van Gammeren, Darin J Falk, Keith C Deruisseau, Melissa A Deering, Tossaporn Yimlamai, Scott K Powers
    Abstract:

    Prolonged Mechanical Ventilation results in diaphragmatic oxidative injury, elevated proteolysis, fiber atrophy, and reduced force-generating capacity. We tested the hypothesis that antioxidant infusion during Mechanical Ventilation would function as an antioxidant to maintain redox balance within diaphragm muscle fibers and therefore prevent oxidative stress and subsequent proteolysis and contractile dysfunction. Sprague-Dawley rats were anesthetized, tracheostomized, and Mechanically ventilated with 21% O2 for 12 hours. The antioxidant Trolox was intravenously infused in a subset of ventilated animals. Compared with acutely anesthetized, nonventilated control animals, Mechanical Ventilation resulted in a significant reduction (–17%) in diaphragmatic maximal tetanic force. Importantly, Trolox completely attenuated this Mechanical Ventilation-induced diaphragmatic contractile deficit. Total diaphragmatic proteolysis was increased 105% in Mechanical Ventilation animals compared with controls. In contrast, ...

  • Trolox Attenuates Mechanical Ventilation–induced Diaphragmatic Dysfunction and Proteolysis
    American Journal of Respiratory and Critical Care Medicine, 2004
    Co-Authors: Jenna L Betters, David S Criswell, Darin Van Gammeren, Darin J Falk, Keith C Deruisseau, Melissa A Deering, Tossaporn Yimlamai, R. Andrew Shanely, Scott K Powers
    Abstract:

    Prolonged Mechanical Ventilation results in diaphragmatic oxidative injury, elevated proteolysis, fiber atrophy, and reduced force-generating capacity. We tested the hypothesis that antioxidant infusion during Mechanical Ventilation would function as an antioxidant to maintain redox balance within diaphragm muscle fibers and therefore prevent oxidative stress and subsequent proteolysis and contractile dysfunction. Sprague-Dawley rats were anesthetized, tracheostomized, and Mechanically ventilated with 21% O2 for 12 hours. The antioxidant Trolox was intravenously infused in a subset of ventilated animals. Compared with acutely anesthetized, nonventilated control animals, Mechanical Ventilation resulted in a significant reduction (–17%) in diaphragmatic maximal tetanic force. Importantly, Trolox completely attenuated this Mechanical Ventilation-induced diaphragmatic contractile deficit. Total diaphragmatic proteolysis was increased 105% in Mechanical Ventilation animals compared with controls. In contrast, ...

Lifu Li - One of the best experts on this subject based on the ideXlab platform.

  • lumican expression in diaphragm induced by Mechanical Ventilation
    PLOS ONE, 2011
    Co-Authors: Cheng-ta Yang, Lifu Li, Baoxiang Chen, Yinghuang Tsai
    Abstract:

    Background Diaphragmatic dysfunction found in the patients with acute lung injury required prolonged Mechanical Ventilation. Mechanical Ventilation can induce production of inflammatory cytokines and excess deposition of extracellular matrix proteins via up-regulation of transforming growth factor (TGF)-β1. Lumican is known to participate in TGF-β1 signaling during wound healing. The mechanisms regulating interactions between Mechanical Ventilation and diaphragmatic injury are unclear. We hypothesized that diaphragmatic damage by short duration of Mechanical stretch caused up-regulation of lumican that modulated TGF-β1 signaling. Methods Male C57BL/6 mice, either wild-type or lumican-null, aged 3 months, weighing between 25 and 30 g, were exposed to normal tidal volume (10 ml/kg) or high tidal volume (30 ml/kg) Mechanical Ventilation with room air for 2 to 8 hours. Nonventilated mice served as control groups. Results High tidal volume Mechanical Ventilation induced interfibrillar disassembly of diaphragmatic collagen fiber, lumican activation, type I and III procollagen, fibronectin, and α-smooth muscle actin (α-SMA) mRNA, production of free radical and TGF-β1 protein, and positive staining of lumican in diaphragmatic fiber. Mechanical Ventilation of lumican deficient mice attenuated diaphragmatic injury, type I and III procollagen, fibronectin, and α-SMA mRNA, and production of free radical and TGF-β1 protein. No significant diaphragmatic injury was found in mice subjected to normal tidal volume Mechanical Ventilation. Conclusion Our data showed that high tidal volume Mechanical Ventilation induced TGF-β1 production, TGF-β1-inducible genes, e.g., collagen, and diaphragmatic dysfunction through activation of the lumican.

Jenna L Betters - One of the best experts on this subject based on the ideXlab platform.

  • trolox attenuates Mechanical Ventilation induced diaphragmatic dysfunction and proteolysis
    American Journal of Respiratory and Critical Care Medicine, 2004
    Co-Authors: Jenna L Betters, David S Criswell, Andrew R Shanely, Darin Van Gammeren, Darin J Falk, Keith C Deruisseau, Melissa A Deering, Tossaporn Yimlamai, Scott K Powers
    Abstract:

    Prolonged Mechanical Ventilation results in diaphragmatic oxidative injury, elevated proteolysis, fiber atrophy, and reduced force-generating capacity. We tested the hypothesis that antioxidant infusion during Mechanical Ventilation would function as an antioxidant to maintain redox balance within diaphragm muscle fibers and therefore prevent oxidative stress and subsequent proteolysis and contractile dysfunction. Sprague-Dawley rats were anesthetized, tracheostomized, and Mechanically ventilated with 21% O2 for 12 hours. The antioxidant Trolox was intravenously infused in a subset of ventilated animals. Compared with acutely anesthetized, nonventilated control animals, Mechanical Ventilation resulted in a significant reduction (–17%) in diaphragmatic maximal tetanic force. Importantly, Trolox completely attenuated this Mechanical Ventilation-induced diaphragmatic contractile deficit. Total diaphragmatic proteolysis was increased 105% in Mechanical Ventilation animals compared with controls. In contrast, ...

  • Trolox Attenuates Mechanical Ventilation–induced Diaphragmatic Dysfunction and Proteolysis
    American Journal of Respiratory and Critical Care Medicine, 2004
    Co-Authors: Jenna L Betters, David S Criswell, Darin Van Gammeren, Darin J Falk, Keith C Deruisseau, Melissa A Deering, Tossaporn Yimlamai, R. Andrew Shanely, Scott K Powers
    Abstract:

    Prolonged Mechanical Ventilation results in diaphragmatic oxidative injury, elevated proteolysis, fiber atrophy, and reduced force-generating capacity. We tested the hypothesis that antioxidant infusion during Mechanical Ventilation would function as an antioxidant to maintain redox balance within diaphragm muscle fibers and therefore prevent oxidative stress and subsequent proteolysis and contractile dysfunction. Sprague-Dawley rats were anesthetized, tracheostomized, and Mechanically ventilated with 21% O2 for 12 hours. The antioxidant Trolox was intravenously infused in a subset of ventilated animals. Compared with acutely anesthetized, nonventilated control animals, Mechanical Ventilation resulted in a significant reduction (–17%) in diaphragmatic maximal tetanic force. Importantly, Trolox completely attenuated this Mechanical Ventilation-induced diaphragmatic contractile deficit. Total diaphragmatic proteolysis was increased 105% in Mechanical Ventilation animals compared with controls. In contrast, ...

Baoxiang Chen - One of the best experts on this subject based on the ideXlab platform.

  • lumican expression in diaphragm induced by Mechanical Ventilation
    PLOS ONE, 2011
    Co-Authors: Cheng-ta Yang, Lifu Li, Baoxiang Chen, Yinghuang Tsai
    Abstract:

    Background Diaphragmatic dysfunction found in the patients with acute lung injury required prolonged Mechanical Ventilation. Mechanical Ventilation can induce production of inflammatory cytokines and excess deposition of extracellular matrix proteins via up-regulation of transforming growth factor (TGF)-β1. Lumican is known to participate in TGF-β1 signaling during wound healing. The mechanisms regulating interactions between Mechanical Ventilation and diaphragmatic injury are unclear. We hypothesized that diaphragmatic damage by short duration of Mechanical stretch caused up-regulation of lumican that modulated TGF-β1 signaling. Methods Male C57BL/6 mice, either wild-type or lumican-null, aged 3 months, weighing between 25 and 30 g, were exposed to normal tidal volume (10 ml/kg) or high tidal volume (30 ml/kg) Mechanical Ventilation with room air for 2 to 8 hours. Nonventilated mice served as control groups. Results High tidal volume Mechanical Ventilation induced interfibrillar disassembly of diaphragmatic collagen fiber, lumican activation, type I and III procollagen, fibronectin, and α-smooth muscle actin (α-SMA) mRNA, production of free radical and TGF-β1 protein, and positive staining of lumican in diaphragmatic fiber. Mechanical Ventilation of lumican deficient mice attenuated diaphragmatic injury, type I and III procollagen, fibronectin, and α-SMA mRNA, and production of free radical and TGF-β1 protein. No significant diaphragmatic injury was found in mice subjected to normal tidal volume Mechanical Ventilation. Conclusion Our data showed that high tidal volume Mechanical Ventilation induced TGF-β1 production, TGF-β1-inducible genes, e.g., collagen, and diaphragmatic dysfunction through activation of the lumican.