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Low altitude simulation without hypoxia improves left ventricular function after myocardial infarction by reducing ventricular afterload
Humans have a lower risk of death from myocardial infarction (MI) living at low elevations (5000 m, and intermittent hypobaric hypoxia post-MI can reduce MI size in rodents, and it is believed that hypoxia is the key stimulus. To explore mechanisms beyond hypoxia we studied whether altitude simulati...
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| Published in: | PloS one 2019-05, Vol.14 (5), p.e0215814-e0215814 |
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| creator | Shahid, Anmol Patel, Vaibhav B Morton, Jude S Stenson, Trevor H Davidge, Sandra T Oudit, Gavin Y McMurtry, Michael S |
| description | Humans have a lower risk of death from myocardial infarction (MI) living at low elevations (5000 m, and intermittent hypobaric hypoxia post-MI can reduce MI size in rodents, and it is believed that hypoxia is the key stimulus. To explore mechanisms beyond hypoxia we studied whether altitude simulation |
| doi_str_mv | 10.1371/journal.pone.0215814 |
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Both chronic hypoxia pre-MI, achieved by altitude simulation >5000 m, and intermittent hypobaric hypoxia post-MI can reduce MI size in rodents, and it is believed that hypoxia is the key stimulus. To explore mechanisms beyond hypoxia we studied whether altitude simulation <2500 m would also be associated with reduced infarct size. We performed left-anterior descending artery ligation on C57BL6 mice. Control mice (n = 12) recovered at 754 mmHg (atmospheric pressure, control), and treatment group mice (n = 13) were placed in a hypobaric chamber to recover 3-hours daily at 714 mmHg for 1 week. Echocardiographic evaluation of left ventricular function was performed on Day 0, Day 1 and Day 8. Intermittent hypobaric treatment was associated with a 14.2±5.3% improvement in ejection fraction for treatment group mice (p<0.01 vs. Day 1), with no change observed in control mice. Cardiac output, stroke volume, and infarct size were also improved in treated mice, but no changes were observed in HIF-1 activation or neovascularization. Next, we studied the acute hemodynamic effects of low altitude stimulation in intact mice breathing 100% oxygen using left ventricular catheterization and recording of pressure-volume loops. Acute reductions in barometric pressure from 754 mmHg to 714 mmHg and 674 mmHg were associated with reduced systemic vascular resistance, increased stroke volume and cardiac output, and no change in blood pressure or heart rate. Ex-vivo vascular function was studied using murine mesenteric artery segments. Acute reductions in barometric pressure were associated with greater vascular distensibility. We conclude that intermittent hypobaric treatment using simulated altitudes <2500 m reduces infarct size and increases ventricular function post-MI, and that these changes are related to altered arterial function and not hypoxia-associated neovascularization.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0215814</identifier><identifier>PMID: 31150412</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Altitude ; Altitude effects ; Altitude simulation ; Animals ; Atmospheric pressure ; Biology and Life Sciences ; Blood pressure ; Cardiac output ; Cardiovascular disease ; Catheterization ; Cerebral infarction ; Consciousness ; Coronary vessels ; Gene Expression Regulation ; Gynecology ; Heart attacks ; Heart failure ; Heart rate ; Hemodynamics ; Hypoxia ; Hypoxia-inducible factor 1 ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Ischemia ; Low altitude ; Medicine ; Medicine and Health Sciences ; Mice ; Mice, Inbred C57BL ; Mortality ; Mouse devices ; Myocardial infarction ; Myocardial Infarction - metabolism ; Myocardial Infarction - physiopathology ; Obstetrics ; Ostomy ; Oxygen ; Physiology ; Polyethylene ; Recording ; Rodent control ; Rodents ; Sea level ; Simulation ; Stroke ; Stroke Volume ; Vascularization ; Ventricle ; Ventricular Function, Left</subject><ispartof>PloS one, 2019-05, Vol.14 (5), p.e0215814-e0215814</ispartof><rights>2019 Shahid et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2019 Shahid et al 2019 Shahid et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c526t-de75345639961cc341028dd2a66a3e13dfde5c2f1a9a2d2f080ea943a9e347733</citedby><cites>FETCH-LOGICAL-c526t-de75345639961cc341028dd2a66a3e13dfde5c2f1a9a2d2f080ea943a9e347733</cites><orcidid>0000-0001-9912-2136 ; 0000-0001-7164-1137 ; 0000-0001-5638-4988</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.proquest.com/docview/2233259002/fulltextPDF?pq-origsite=primo$$EPDF$$P50$$Gproquest$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.proquest.com/docview/2233259002?pq-origsite=primo$$EHTML$$P50$$Gproquest$$Hfree_for_read</linktohtml><link.rule.ids>230,314,727,780,784,885,25751,27922,27923,37010,37011,44588,53789,53791,74896</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31150412$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Lionetti, Vincenzo</contributor><creatorcontrib>Shahid, Anmol</creatorcontrib><creatorcontrib>Patel, Vaibhav B</creatorcontrib><creatorcontrib>Morton, Jude S</creatorcontrib><creatorcontrib>Stenson, Trevor H</creatorcontrib><creatorcontrib>Davidge, Sandra T</creatorcontrib><creatorcontrib>Oudit, Gavin Y</creatorcontrib><creatorcontrib>McMurtry, Michael S</creatorcontrib><title>Low altitude simulation without hypoxia improves left ventricular function after myocardial infarction by reducing ventricular afterload</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Humans have a lower risk of death from myocardial infarction (MI) living at low elevations (<2500 m), which are not high enough to induce hypoxia. Both chronic hypoxia pre-MI, achieved by altitude simulation >5000 m, and intermittent hypobaric hypoxia post-MI can reduce MI size in rodents, and it is believed that hypoxia is the key stimulus. To explore mechanisms beyond hypoxia we studied whether altitude simulation <2500 m would also be associated with reduced infarct size. We performed left-anterior descending artery ligation on C57BL6 mice. Control mice (n = 12) recovered at 754 mmHg (atmospheric pressure, control), and treatment group mice (n = 13) were placed in a hypobaric chamber to recover 3-hours daily at 714 mmHg for 1 week. Echocardiographic evaluation of left ventricular function was performed on Day 0, Day 1 and Day 8. Intermittent hypobaric treatment was associated with a 14.2±5.3% improvement in ejection fraction for treatment group mice (p<0.01 vs. Day 1), with no change observed in control mice. Cardiac output, stroke volume, and infarct size were also improved in treated mice, but no changes were observed in HIF-1 activation or neovascularization. Next, we studied the acute hemodynamic effects of low altitude stimulation in intact mice breathing 100% oxygen using left ventricular catheterization and recording of pressure-volume loops. Acute reductions in barometric pressure from 754 mmHg to 714 mmHg and 674 mmHg were associated with reduced systemic vascular resistance, increased stroke volume and cardiac output, and no change in blood pressure or heart rate. Ex-vivo vascular function was studied using murine mesenteric artery segments. Acute reductions in barometric pressure were associated with greater vascular distensibility. We conclude that intermittent hypobaric treatment using simulated altitudes <2500 m reduces infarct size and increases ventricular function post-MI, and that these changes are related to altered arterial function and not hypoxia-associated neovascularization.</description><subject>Altitude</subject><subject>Altitude effects</subject><subject>Altitude simulation</subject><subject>Animals</subject><subject>Atmospheric pressure</subject><subject>Biology and Life Sciences</subject><subject>Blood pressure</subject><subject>Cardiac output</subject><subject>Cardiovascular disease</subject><subject>Catheterization</subject><subject>Cerebral infarction</subject><subject>Consciousness</subject><subject>Coronary vessels</subject><subject>Gene Expression Regulation</subject><subject>Gynecology</subject><subject>Heart attacks</subject><subject>Heart failure</subject><subject>Heart rate</subject><subject>Hemodynamics</subject><subject>Hypoxia</subject><subject>Hypoxia-inducible factor 1</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Ischemia</subject><subject>Low altitude</subject><subject>Medicine</subject><subject>Medicine and Health Sciences</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mortality</subject><subject>Mouse devices</subject><subject>Myocardial infarction</subject><subject>Myocardial Infarction - metabolism</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Obstetrics</subject><subject>Ostomy</subject><subject>Oxygen</subject><subject>Physiology</subject><subject>Polyethylene</subject><subject>Recording</subject><subject>Rodent control</subject><subject>Rodents</subject><subject>Sea level</subject><subject>Simulation</subject><subject>Stroke</subject><subject>Stroke Volume</subject><subject>Vascularization</subject><subject>Ventricle</subject><subject>Ventricular Function, 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altitude simulation without hypoxia improves left ventricular function after myocardial infarction by reducing ventricular afterload</title><author>Shahid, Anmol ; Patel, Vaibhav B ; Morton, Jude S ; Stenson, Trevor H ; Davidge, Sandra T ; Oudit, Gavin Y ; McMurtry, Michael S</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c526t-de75345639961cc341028dd2a66a3e13dfde5c2f1a9a2d2f080ea943a9e347733</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2019</creationdate><topic>Altitude</topic><topic>Altitude effects</topic><topic>Altitude simulation</topic><topic>Animals</topic><topic>Atmospheric pressure</topic><topic>Biology and Life Sciences</topic><topic>Blood pressure</topic><topic>Cardiac output</topic><topic>Cardiovascular disease</topic><topic>Catheterization</topic><topic>Cerebral infarction</topic><topic>Consciousness</topic><topic>Coronary vessels</topic><topic>Gene Expression 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low elevations (<2500 m), which are not high enough to induce hypoxia. Both chronic hypoxia pre-MI, achieved by altitude simulation >5000 m, and intermittent hypobaric hypoxia post-MI can reduce MI size in rodents, and it is believed that hypoxia is the key stimulus. To explore mechanisms beyond hypoxia we studied whether altitude simulation <2500 m would also be associated with reduced infarct size. We performed left-anterior descending artery ligation on C57BL6 mice. Control mice (n = 12) recovered at 754 mmHg (atmospheric pressure, control), and treatment group mice (n = 13) were placed in a hypobaric chamber to recover 3-hours daily at 714 mmHg for 1 week. Echocardiographic evaluation of left ventricular function was performed on Day 0, Day 1 and Day 8. Intermittent hypobaric treatment was associated with a 14.2±5.3% improvement in ejection fraction for treatment group mice (p<0.01 vs. Day 1), with no change observed in control mice. Cardiac output, stroke volume, and infarct size were also improved in treated mice, but no changes were observed in HIF-1 activation or neovascularization. Next, we studied the acute hemodynamic effects of low altitude stimulation in intact mice breathing 100% oxygen using left ventricular catheterization and recording of pressure-volume loops. Acute reductions in barometric pressure from 754 mmHg to 714 mmHg and 674 mmHg were associated with reduced systemic vascular resistance, increased stroke volume and cardiac output, and no change in blood pressure or heart rate. Ex-vivo vascular function was studied using murine mesenteric artery segments. Acute reductions in barometric pressure were associated with greater vascular distensibility. We conclude that intermittent hypobaric treatment using simulated altitudes <2500 m reduces infarct size and increases ventricular function post-MI, and that these changes are related to altered arterial function and not hypoxia-associated neovascularization.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>31150412</pmid><doi>10.1371/journal.pone.0215814</doi><orcidid>https://orcid.org/0000-0001-9912-2136</orcidid><orcidid>https://orcid.org/0000-0001-7164-1137</orcidid><orcidid>https://orcid.org/0000-0001-5638-4988</orcidid><oa>free_for_read</oa></addata></record> |
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| identifier | ISSN: 1932-6203 |
| ispartof | PloS one, 2019-05, Vol.14 (5), p.e0215814-e0215814 |
| issn | 1932-6203 1932-6203 |
| language | eng |
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| source | Publicly Available Content Database; PubMed Central |
| subjects | Altitude Altitude effects Altitude simulation Animals Atmospheric pressure Biology and Life Sciences Blood pressure Cardiac output Cardiovascular disease Catheterization Cerebral infarction Consciousness Coronary vessels Gene Expression Regulation Gynecology Heart attacks Heart failure Heart rate Hemodynamics Hypoxia Hypoxia-inducible factor 1 Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Ischemia Low altitude Medicine Medicine and Health Sciences Mice Mice, Inbred C57BL Mortality Mouse devices Myocardial infarction Myocardial Infarction - metabolism Myocardial Infarction - physiopathology Obstetrics Ostomy Oxygen Physiology Polyethylene Recording Rodent control Rodents Sea level Simulation Stroke Stroke Volume Vascularization Ventricle Ventricular Function, Left |
| title | Low altitude simulation without hypoxia improves left ventricular function after myocardial infarction by reducing ventricular afterload |
| url | http://sfxeu10.hosted.exlibrisgroup.com/loughborough?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-14T13%3A54%3A26IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_plos_&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Low%20altitude%20simulation%20without%20hypoxia%20improves%20left%20ventricular%20function%20after%20myocardial%20infarction%20by%20reducing%20ventricular%20afterload&rft.jtitle=PloS%20one&rft.au=Shahid,%20Anmol&rft.date=2019-05-31&rft.volume=14&rft.issue=5&rft.spage=e0215814&rft.epage=e0215814&rft.pages=e0215814-e0215814&rft.issn=1932-6203&rft.eissn=1932-6203&rft_id=info:doi/10.1371/journal.pone.0215814&rft_dat=%3Cproquest_plos_%3E2233856050%3C/proquest_plos_%3E%3Cgrp_id%3Ecdi_FETCH-LOGICAL-c526t-de75345639961cc341028dd2a66a3e13dfde5c2f1a9a2d2f080ea943a9e347733%3C/grp_id%3E%3Coa%3E%3C/oa%3E%3Curl%3E%3C/url%3E&rft_id=info:oai/&rft_pqid=2233259002&rft_id=info:pmid/31150412&rfr_iscdi=true |