Angiotensin 1‐7 protects against ventilator‐induced diaphragm dysfunction
Mechanical ventilation (MV) is a life‐saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery. Unfortunately, an unintended consequence of prolonged MV is the development of inspiratory weakness due to both diaphragmatic atrophy and contracti...
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Published in | Clinical and translational science Vol. 14; no. 4; pp. 1512 - 1523 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
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United States
John Wiley & Sons, Inc
01.07.2021
John Wiley and Sons Inc Wiley |
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Abstract | Mechanical ventilation (MV) is a life‐saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery. Unfortunately, an unintended consequence of prolonged MV is the development of inspiratory weakness due to both diaphragmatic atrophy and contractile dysfunction; this syndrome is labeled ventilator‐induced diaphragm dysfunction (VIDD). VIDD is clinically important because diaphragmatic weakness is an important contributor to problems in weaning patients from MV. Investigations into the pathogenesis of VIDD reveal that oxidative stress is essential for the rapid development of VIDD as redox disturbances in diaphragm fibers promote accelerated proteolysis. Currently, no standard treatment exists to prevent VIDD and, therefore, developing a strategy to avert VIDD is vital. Guided by evidence indicating that activation of the classical axis of the renin‐angiotensin system (RAS) in diaphragm fibers promotes oxidative stress and VIDD, we hypothesized that activation of the nonclassical RAS signaling pathway via angiotensin 1‐7 (Ang1‐7) will protect against VIDD. Using an established animal model of prolonged MV, our results disclose that infusion of Ang1‐7 protects the diaphragm against MV‐induced contractile dysfunction and fiber atrophy in both fast and slow muscle fibers. Further, Ang1‐7 shielded diaphragm fibers against MV‐induced mitochondrial damage, oxidative stress, and protease activation. Collectively, these results reveal that treatment with Ang1‐7 protects against VIDD, in part, due to diminishing oxidative stress and protease activation. These important findings provide robust evidence that Ang1‐7 has the therapeutic potential to protect against VIDD by preventing MV‐induced contractile dysfunction and atrophy of both slow and fast muscle fibers. |
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AbstractList | Mechanical ventilation (MV) is a life-saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery. Unfortunately, an unintended consequence of prolonged MV is the development of inspiratory weakness due to both diaphragmatic atrophy and contractile dysfunction; this syndrome is labeled ventilator-induced diaphragm dysfunction (VIDD). VIDD is clinically important because diaphragmatic weakness is an important contributor to problems in weaning patients from MV. Investigations into the pathogenesis of VIDD reveal that oxidative stress is essential for the rapid development of VIDD as redox disturbances in diaphragm fibers promote accelerated proteolysis. Currently, no standard treatment exists to prevent VIDD and, therefore, developing a strategy to avert VIDD is vital. Guided by evidence indicating that activation of the classical axis of the renin-angiotensin system (RAS) in diaphragm fibers promotes oxidative stress and VIDD, we hypothesized that activation of the nonclassical RAS signaling pathway via angiotensin 1-7 (Ang1-7) will protect against VIDD. Using an established animal model of prolonged MV, our results disclose that infusion of Ang1-7 protects the diaphragm against MV-induced contractile dysfunction and fiber atrophy in both fast and slow muscle fibers. Further, Ang1-7 shielded diaphragm fibers against MV-induced mitochondrial damage, oxidative stress, and protease activation. Collectively, these results reveal that treatment with Ang1-7 protects against VIDD, in part, due to diminishing oxidative stress and protease activation. These important findings provide robust evidence that Ang1-7 has the therapeutic potential to protect against VIDD by preventing MV-induced contractile dysfunction and atrophy of both slow and fast muscle fibers. Abstract Mechanical ventilation (MV) is a life‐saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery. Unfortunately, an unintended consequence of prolonged MV is the development of inspiratory weakness due to both diaphragmatic atrophy and contractile dysfunction; this syndrome is labeled ventilator‐induced diaphragm dysfunction (VIDD). VIDD is clinically important because diaphragmatic weakness is an important contributor to problems in weaning patients from MV. Investigations into the pathogenesis of VIDD reveal that oxidative stress is essential for the rapid development of VIDD as redox disturbances in diaphragm fibers promote accelerated proteolysis. Currently, no standard treatment exists to prevent VIDD and, therefore, developing a strategy to avert VIDD is vital. Guided by evidence indicating that activation of the classical axis of the renin‐angiotensin system (RAS) in diaphragm fibers promotes oxidative stress and VIDD, we hypothesized that activation of the nonclassical RAS signaling pathway via angiotensin 1‐7 (Ang1‐7) will protect against VIDD. Using an established animal model of prolonged MV, our results disclose that infusion of Ang1‐7 protects the diaphragm against MV‐induced contractile dysfunction and fiber atrophy in both fast and slow muscle fibers. Further, Ang1‐7 shielded diaphragm fibers against MV‐induced mitochondrial damage, oxidative stress, and protease activation. Collectively, these results reveal that treatment with Ang1‐7 protects against VIDD, in part, due to diminishing oxidative stress and protease activation. These important findings provide robust evidence that Ang1‐7 has the therapeutic potential to protect against VIDD by preventing MV‐induced contractile dysfunction and atrophy of both slow and fast muscle fibers. |
Author | Nguyen, Branden L. Ozdemir, Mustafa Powers, Scott K. Deminice, Rafael Yoshihara, Toshinori Hyatt, Hayden W. |
AuthorAffiliation | 1 Department of Applied Physiology and Kinesiology University of Florida Gainesville Florida USA 2 Graduate School of Health and Sports Science Juntendo University Inzai Japan 3 Department of Physical Education State University of Londrina Londrina Brazil |
AuthorAffiliation_xml | – name: 1 Department of Applied Physiology and Kinesiology University of Florida Gainesville Florida USA – name: 2 Graduate School of Health and Sports Science Juntendo University Inzai Japan – name: 3 Department of Physical Education State University of Londrina Londrina Brazil |
Author_xml | – sequence: 1 givenname: Toshinori surname: Yoshihara fullname: Yoshihara, Toshinori email: t-yoshih@juntendo.ac.jp organization: Juntendo University – sequence: 2 givenname: Rafael surname: Deminice fullname: Deminice, Rafael organization: State University of Londrina – sequence: 3 givenname: Hayden W. surname: Hyatt fullname: Hyatt, Hayden W. organization: University of Florida – sequence: 4 givenname: Mustafa surname: Ozdemir fullname: Ozdemir, Mustafa organization: University of Florida – sequence: 5 givenname: Branden L. surname: Nguyen fullname: Nguyen, Branden L. organization: University of Florida – sequence: 6 givenname: Scott K. surname: Powers fullname: Powers, Scott K. organization: University of Florida |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/33742769$$D View this record in MEDLINE/PubMed |
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CitedBy_id | crossref_primary_10_2174_1566524021666211207112106 crossref_primary_10_1186_s12890_023_02662_7 crossref_primary_10_1186_s13395_022_00304_w |
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Snippet | Mechanical ventilation (MV) is a life‐saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery.... Mechanical ventilation (MV) is a life-saving instrument used to provide ventilatory support for critically ill patients and patients undergoing surgery.... Abstract Mechanical ventilation (MV) is a life‐saving instrument used to provide ventilatory support for critically ill patients and patients undergoing... |
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SubjectTerms | Angiotensin Angiotensin I - administration & dosage Animal models Animals Atrophy Blood pressure Catheters Diaphragm Diaphragm (Anatomy) Diaphragm - drug effects Diaphragm - physiopathology Disease Models, Animal Endocrine system Experiments Female Force Humans Infusions, Intravenous Mechanical ventilation Mitochondria Muscle contraction Muscle Contraction - drug effects Muscle Contraction - physiology Muscle Weakness - etiology Muscle Weakness - physiopathology Muscle Weakness - prevention & control Muscular Disorders, Atrophic - etiology Muscular Disorders, Atrophic - physiopathology Muscular Disorders, Atrophic - prevention & control Oxidative stress Oxidative Stress - drug effects Patients Peptide Fragments - administration & dosage Proteinase Proteolysis Rats Renin Respiration Respiration, Artificial - adverse effects Signal transduction Ventilators Weaning |
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Title | Angiotensin 1‐7 protects against ventilator‐induced diaphragm dysfunction |
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