Hyperbaric therapy provides no benefit for skeletal muscle and respiratory function and accelerates cardiac injury in mdx mice
Duchenne muscular dystrophy (DMD) is a uniformly fatal condition of striated muscle wasting resulting in premature death from respiratory and/or cardiac failure. Symptomatic therapy has prolonged survival by limiting deaths resulting from respiratory insufficiency, but there is currently no effectiv...
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description | Duchenne muscular dystrophy (DMD) is a uniformly fatal condition of striated muscle wasting resulting in premature death from respiratory and/or cardiac failure. Symptomatic therapy has prolonged survival by limiting deaths resulting from respiratory insufficiency, but there is currently no effective therapy for most patients with DMD. This grim prognosis has led patients and their families to seek unproven therapeutic approaches. One such approach is the use of hyperbaric therapies, which 14% of DMD patients self-report using. The primary goal of this study was to determine if intermittent hyperbaric exposure altered the muscle function of the mdx mouse, a genetic model of DMD. To do this, mdx mice were exposed to three daily 90-minute 1.3 atmosphere hyperbaric exposures for 4 weeks. Skeletal muscle, respiratory, and cardiac function were assessed in treated and untreated wild type and dystrophic mice. The results of these studies find that hyperbaric and hyperoxic approaches resulted in increased cardiac fibrosis in dystrophic mice and no beneficial effects on the functional parameters measured. These data suggest that these oxygen-based therapies are unlikely to provide therapeutic benefit to DMD patients. |
doi_str_mv | 10.1038/s41598-019-48744-7 |
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Symptomatic therapy has prolonged survival by limiting deaths resulting from respiratory insufficiency, but there is currently no effective therapy for most patients with DMD. This grim prognosis has led patients and their families to seek unproven therapeutic approaches. One such approach is the use of hyperbaric therapies, which 14% of DMD patients self-report using. The primary goal of this study was to determine if intermittent hyperbaric exposure altered the muscle function of the mdx mouse, a genetic model of DMD. To do this, mdx mice were exposed to three daily 90-minute 1.3 atmosphere hyperbaric exposures for 4 weeks. Skeletal muscle, respiratory, and cardiac function were assessed in treated and untreated wild type and dystrophic mice. The results of these studies find that hyperbaric and hyperoxic approaches resulted in increased cardiac fibrosis in dystrophic mice and no beneficial effects on the functional parameters measured. These data suggest that these oxygen-based therapies are unlikely to provide therapeutic benefit to DMD patients.</description><identifier>ISSN: 2045-2322</identifier><identifier>EISSN: 2045-2322</identifier><identifier>DOI: 10.1038/s41598-019-48744-7</identifier><identifier>PMID: 31444390</identifier><language>eng</language><publisher>London: Nature Publishing Group UK</publisher><subject>631/443/592/75/74 ; 64 ; 64/60 ; 692/617/375/374 ; Animals ; Duchenne's muscular dystrophy ; Dystrophy ; Fibrosis ; Hand Strength ; Heart - physiopathology ; Heart Injuries - etiology ; Heart Injuries - physiopathology ; Hemodynamics ; Humanities and Social Sciences ; Hyperbaric Oxygenation - adverse effects ; Hyperoxia - physiopathology ; Male ; Medical prognosis ; Mice, Inbred C57BL ; Mice, Inbred mdx ; multidisciplinary ; Muscle, Skeletal - physiopathology ; Muscular Dystrophy, Duchenne - pathology ; Muscular Dystrophy, Duchenne - physiopathology ; Musculoskeletal system ; Physical Conditioning, Animal ; Plethysmography ; Pressure ; Respiration ; Respiratory function ; Rodents ; Science ; Science (multidisciplinary) ; Skeletal muscle</subject><ispartof>Scientific reports, 2019-08, Vol.9 (1), p.12306-10, Article 12306</ispartof><rights>The Author(s) 2019</rights><rights>2019. 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Symptomatic therapy has prolonged survival by limiting deaths resulting from respiratory insufficiency, but there is currently no effective therapy for most patients with DMD. This grim prognosis has led patients and their families to seek unproven therapeutic approaches. One such approach is the use of hyperbaric therapies, which 14% of DMD patients self-report using. The primary goal of this study was to determine if intermittent hyperbaric exposure altered the muscle function of the mdx mouse, a genetic model of DMD. To do this, mdx mice were exposed to three daily 90-minute 1.3 atmosphere hyperbaric exposures for 4 weeks. Skeletal muscle, respiratory, and cardiac function were assessed in treated and untreated wild type and dystrophic mice. The results of these studies find that hyperbaric and hyperoxic approaches resulted in increased cardiac fibrosis in dystrophic mice and no beneficial effects on the functional parameters measured. These data suggest that these oxygen-based therapies are unlikely to provide therapeutic benefit to DMD patients.</description><subject>631/443/592/75/74</subject><subject>64</subject><subject>64/60</subject><subject>692/617/375/374</subject><subject>Animals</subject><subject>Duchenne's muscular dystrophy</subject><subject>Dystrophy</subject><subject>Fibrosis</subject><subject>Hand Strength</subject><subject>Heart - physiopathology</subject><subject>Heart Injuries - etiology</subject><subject>Heart Injuries - physiopathology</subject><subject>Hemodynamics</subject><subject>Humanities and Social Sciences</subject><subject>Hyperbaric Oxygenation - adverse effects</subject><subject>Hyperoxia - physiopathology</subject><subject>Male</subject><subject>Medical prognosis</subject><subject>Mice, Inbred C57BL</subject><subject>Mice, Inbred mdx</subject><subject>multidisciplinary</subject><subject>Muscle, Skeletal - physiopathology</subject><subject>Muscular Dystrophy, Duchenne - pathology</subject><subject>Muscular Dystrophy, Duchenne - physiopathology</subject><subject>Musculoskeletal system</subject><subject>Physical Conditioning, Animal</subject><subject>Plethysmography</subject><subject>Pressure</subject><subject>Respiration</subject><subject>Respiratory function</subject><subject>Rodents</subject><subject>Science</subject><subject>Science (multidisciplinary)</subject><subject>Skeletal muscle</subject><issn>2045-2322</issn><issn>2045-2322</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2019</creationdate><recordtype>article</recordtype><sourceid>C6C</sourceid><sourceid>EIF</sourceid><sourceid>BENPR</sourceid><recordid>eNp9kU9rFTEUxQdRbKn9Ai4k4MbNaP5Oko0gRa1QcKPrkElu2jxnkjGZKb6Nn920r9bqwmwSOL97bg6n654T_Jpgpt5UToRWPSa650py3stH3THFXPSUUfr4wfuoO611h9sRVHOin3ZHjHDOmcbH3c_z_QJltCU6tF5BscseLSVfRw8VpYxGSBDiikIuqH6DCVY7oXmrbgJkk0cF6hKLXXPZo7Alt8acbgXrXKOb0nycLT5ah2LabY2LCc3-B5qjg2fdk2CnCqd390n39cP7L2fn_cXnj5_O3l30jku-9t7Z0WkM3AO1A3PYB6ZAKQlDoFJbTYAONAisR0pAKPBkDFhwq9gwBufYSff24Lts4wzeQVqLncxS4mzL3mQbzd9KilfmMl-bQWJJB9EMXt0ZlPx9g7qaOdaWcLIJ8lYNpUoKorjEDX35D7rLW0ktXqOkGhgX-oaiB8qVXGuBcP8Zgs1Nw-bQsGkNm9uGjWxDLx7GuB_53WcD2AGoTUqXUP7s_o_tLwC5tSY</recordid><startdate>20190823</startdate><enddate>20190823</enddate><creator>Fischer, Kaleb D.</creator><creator>Heitzman, Jackie A.</creator><creator>Townsend, DeWayne</creator><general>Nature Publishing Group UK</general><general>Nature Publishing Group</general><scope>C6C</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>88A</scope><scope>88E</scope><scope>88I</scope><scope>8FE</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BHPHI</scope><scope>CCPQU</scope><scope>DWQXO</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M2P</scope><scope>M7P</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>Q9U</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20190823</creationdate><title>Hyperbaric therapy provides no benefit for skeletal muscle and respiratory function and accelerates cardiac injury in mdx mice</title><author>Fischer, Kaleb D. ; Heitzman, Jackie A. ; Townsend, DeWayne</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c474t-dcabc90e4de2a63c0df38e887e6f279a91e262f509b21e58ed1bf054a836bfcc3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>631/443/592/75/74</topic><topic>64</topic><topic>64/60</topic><topic>692/617/375/374</topic><topic>Animals</topic><topic>Duchenne's muscular dystrophy</topic><topic>Dystrophy</topic><topic>Fibrosis</topic><topic>Hand Strength</topic><topic>Heart - physiopathology</topic><topic>Heart Injuries - etiology</topic><topic>Heart Injuries - physiopathology</topic><topic>Hemodynamics</topic><topic>Humanities and Social Sciences</topic><topic>Hyperbaric Oxygenation - adverse effects</topic><topic>Hyperoxia - physiopathology</topic><topic>Male</topic><topic>Medical prognosis</topic><topic>Mice, Inbred C57BL</topic><topic>Mice, Inbred mdx</topic><topic>multidisciplinary</topic><topic>Muscle, Skeletal - physiopathology</topic><topic>Muscular Dystrophy, Duchenne - pathology</topic><topic>Muscular Dystrophy, Duchenne - physiopathology</topic><topic>Musculoskeletal system</topic><topic>Physical Conditioning, Animal</topic><topic>Plethysmography</topic><topic>Pressure</topic><topic>Respiration</topic><topic>Respiratory function</topic><topic>Rodents</topic><topic>Science</topic><topic>Science (multidisciplinary)</topic><topic>Skeletal muscle</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Fischer, Kaleb D.</creatorcontrib><creatorcontrib>Heitzman, Jackie A.</creatorcontrib><creatorcontrib>Townsend, DeWayne</creatorcontrib><collection>Springer Nature OA/Free Journals</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Biology Database (Alumni Edition)</collection><collection>Medical Database (Alumni Edition)</collection><collection>Science Database (Alumni Edition)</collection><collection>ProQuest SciTech Collection</collection><collection>ProQuest Natural Science Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest One Sustainability</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central Essentials</collection><collection>Biological Science Collection</collection><collection>ProQuest Central</collection><collection>Natural Science Collection</collection><collection>ProQuest One Community College</collection><collection>ProQuest Central Korea</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Central Student</collection><collection>SciTech Premium Collection</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>ProQuest Biological Science Collection</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>Science Database</collection><collection>Biological Science Database</collection><collection>Publicly Available Content Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central Basic</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Scientific reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Fischer, Kaleb D.</au><au>Heitzman, Jackie A.</au><au>Townsend, DeWayne</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hyperbaric therapy provides no benefit for skeletal muscle and respiratory function and accelerates cardiac injury in mdx mice</atitle><jtitle>Scientific reports</jtitle><stitle>Sci Rep</stitle><addtitle>Sci Rep</addtitle><date>2019-08-23</date><risdate>2019</risdate><volume>9</volume><issue>1</issue><spage>12306</spage><epage>10</epage><pages>12306-10</pages><artnum>12306</artnum><issn>2045-2322</issn><eissn>2045-2322</eissn><abstract>Duchenne muscular dystrophy (DMD) is a uniformly fatal condition of striated muscle wasting resulting in premature death from respiratory and/or cardiac failure. Symptomatic therapy has prolonged survival by limiting deaths resulting from respiratory insufficiency, but there is currently no effective therapy for most patients with DMD. This grim prognosis has led patients and their families to seek unproven therapeutic approaches. One such approach is the use of hyperbaric therapies, which 14% of DMD patients self-report using. The primary goal of this study was to determine if intermittent hyperbaric exposure altered the muscle function of the mdx mouse, a genetic model of DMD. To do this, mdx mice were exposed to three daily 90-minute 1.3 atmosphere hyperbaric exposures for 4 weeks. Skeletal muscle, respiratory, and cardiac function were assessed in treated and untreated wild type and dystrophic mice. The results of these studies find that hyperbaric and hyperoxic approaches resulted in increased cardiac fibrosis in dystrophic mice and no beneficial effects on the functional parameters measured. These data suggest that these oxygen-based therapies are unlikely to provide therapeutic benefit to DMD patients.</abstract><cop>London</cop><pub>Nature Publishing Group UK</pub><pmid>31444390</pmid><doi>10.1038/s41598-019-48744-7</doi><tpages>10</tpages><oa>free_for_read</oa></addata></record> |
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subjects | 631/443/592/75/74 64 64/60 692/617/375/374 Animals Duchenne's muscular dystrophy Dystrophy Fibrosis Hand Strength Heart - physiopathology Heart Injuries - etiology Heart Injuries - physiopathology Hemodynamics Humanities and Social Sciences Hyperbaric Oxygenation - adverse effects Hyperoxia - physiopathology Male Medical prognosis Mice, Inbred C57BL Mice, Inbred mdx multidisciplinary Muscle, Skeletal - physiopathology Muscular Dystrophy, Duchenne - pathology Muscular Dystrophy, Duchenne - physiopathology Musculoskeletal system Physical Conditioning, Animal Plethysmography Pressure Respiration Respiratory function Rodents Science Science (multidisciplinary) Skeletal muscle |
title | Hyperbaric therapy provides no benefit for skeletal muscle and respiratory function and accelerates cardiac injury in mdx mice |
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