Reduced Epicardial Vagal Nerve Density and Impaired Vagal Control in a Rat Myocardial Infarction-Heart Failure Model
Abstract Background Autonomic remodeling, characterized by sympathetic activation and vagal withdrawal, contributes to heart failure (HF) progression. However, the exact mechanism(s) responsible for vagal withdrawal in HF remain(s) unclear, and whether HF causes epicardial autonomic nerve remodeling...
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| Veröffentlicht in: | Cardiovascular pathology 2017-01, Vol.26, p.21-29 |
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| creator | Delfiner, Matthew S Siano, John Li, Ying Dedkov, Eduard I Zhang, Youhua |
| description | Abstract Background Autonomic remodeling, characterized by sympathetic activation and vagal withdrawal, contributes to heart failure (HF) progression. However, the exact mechanism(s) responsible for vagal withdrawal in HF remain(s) unclear, and whether HF causes epicardial autonomic nerve remodeling is unknown. Methods and Results Myocardial infarction (MI) was produced in 14 Sprague–Dawley rats, and 10 sham surgery rats served as the control. MI-HF was confirmed 2 months after the surgery by echocardiography and hemodynamic measurement. Cervical vagal nerve stimulation was delivered to examine the heart rate slowing effect. Whole heart acetylcholinesterase histochemistry was used to examine the epicardial autonomic nerve remodeling at dorsal ventricles (remote from the infarcted area). Compared with the control animals, the same vagal nerve stimulation had less heart rate slowing effect in MI-HF group. Both epicardial nerve bundle length-density (2.56±0.60 μm/mm2 versus 1.68±0.46 μm/mm2 , P =.001) and branching point-density (1.24±0.25 points/mm2 versus 0.66±0.18 points/ mm2 , P |
| doi_str_mv | 10.1016/j.carpath.2016.10.003 |
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However, the exact mechanism(s) responsible for vagal withdrawal in HF remain(s) unclear, and whether HF causes epicardial autonomic nerve remodeling is unknown. Methods and Results Myocardial infarction (MI) was produced in 14 Sprague–Dawley rats, and 10 sham surgery rats served as the control. MI-HF was confirmed 2 months after the surgery by echocardiography and hemodynamic measurement. Cervical vagal nerve stimulation was delivered to examine the heart rate slowing effect. Whole heart acetylcholinesterase histochemistry was used to examine the epicardial autonomic nerve remodeling at dorsal ventricles (remote from the infarcted area). Compared with the control animals, the same vagal nerve stimulation had less heart rate slowing effect in MI-HF group. Both epicardial nerve bundle length-density (2.56±0.60 μm/mm2 versus 1.68±0.46 μm/mm2 , P =.001) and branching point-density (1.24±0.25 points/mm2 versus 0.66±0.18 points/ mm2 , P <.001) were lower in MI-HF rats. The chemically stained epicardial nerve bundles contain both sympathetic (tyrosine hydroxylase positive) and vagal (choline acetyltransferase positive) fibers. However within the stained nerve bundle, the chemical color corresponds mainly with the vagal fibers. Conclusions Whole heart acetylcholinesterase histochemistry revealed a decreased ventricular epicardial vagal nerve density in MI-HF rats, which may contribute to impaired cardiac vagal control in HF.</description><identifier>ISSN: 1054-8807</identifier><identifier>EISSN: 1879-1336</identifier><identifier>DOI: 10.1016/j.carpath.2016.10.003</identifier><identifier>PMID: 27852001</identifier><language>eng</language><publisher>United States: Elsevier Inc</publisher><subject>Acetylcholinesterase - analysis ; Animals ; Autonomic nervous system ; Autonomic Nervous System - physiopathology ; Disease Models, Animal ; Epicardial nerve bundle ; Female ; Heart failure ; Heart Failure - physiopathology ; Immunohistochemistry ; Male ; Myocardial Infarction - physiopathology ; Pathology ; Pericardium - innervation ; Rats ; Rats, Sprague-Dawley ; Vagal nerve ; Vagus Nerve - pathology</subject><ispartof>Cardiovascular pathology, 2017-01, Vol.26, p.21-29</ispartof><rights>2016 Elsevier Inc.</rights><rights>Copyright © 2016 Elsevier Inc. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c420t-c29da6b24757893ab7242fae96779259f1ad87ce8988b48616fb5274f981f2053</citedby><cites>FETCH-LOGICAL-c420t-c29da6b24757893ab7242fae96779259f1ad87ce8988b48616fb5274f981f2053</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.carpath.2016.10.003$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3541,27915,27916,45986</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27852001$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Delfiner, Matthew S</creatorcontrib><creatorcontrib>Siano, John</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Dedkov, Eduard I</creatorcontrib><creatorcontrib>Zhang, Youhua</creatorcontrib><title>Reduced Epicardial Vagal Nerve Density and Impaired Vagal Control in a Rat Myocardial Infarction-Heart Failure Model</title><title>Cardiovascular pathology</title><addtitle>Cardiovasc Pathol</addtitle><description>Abstract Background Autonomic remodeling, characterized by sympathetic activation and vagal withdrawal, contributes to heart failure (HF) progression. However, the exact mechanism(s) responsible for vagal withdrawal in HF remain(s) unclear, and whether HF causes epicardial autonomic nerve remodeling is unknown. Methods and Results Myocardial infarction (MI) was produced in 14 Sprague–Dawley rats, and 10 sham surgery rats served as the control. MI-HF was confirmed 2 months after the surgery by echocardiography and hemodynamic measurement. Cervical vagal nerve stimulation was delivered to examine the heart rate slowing effect. Whole heart acetylcholinesterase histochemistry was used to examine the epicardial autonomic nerve remodeling at dorsal ventricles (remote from the infarcted area). Compared with the control animals, the same vagal nerve stimulation had less heart rate slowing effect in MI-HF group. Both epicardial nerve bundle length-density (2.56±0.60 μm/mm2 versus 1.68±0.46 μm/mm2 , P =.001) and branching point-density (1.24±0.25 points/mm2 versus 0.66±0.18 points/ mm2 , P <.001) were lower in MI-HF rats. The chemically stained epicardial nerve bundles contain both sympathetic (tyrosine hydroxylase positive) and vagal (choline acetyltransferase positive) fibers. However within the stained nerve bundle, the chemical color corresponds mainly with the vagal fibers. Conclusions Whole heart acetylcholinesterase histochemistry revealed a decreased ventricular epicardial vagal nerve density in MI-HF rats, which may contribute to impaired cardiac vagal control in HF.</description><subject>Acetylcholinesterase - analysis</subject><subject>Animals</subject><subject>Autonomic nervous system</subject><subject>Autonomic Nervous System - physiopathology</subject><subject>Disease Models, Animal</subject><subject>Epicardial nerve bundle</subject><subject>Female</subject><subject>Heart failure</subject><subject>Heart Failure - physiopathology</subject><subject>Immunohistochemistry</subject><subject>Male</subject><subject>Myocardial Infarction - physiopathology</subject><subject>Pathology</subject><subject>Pericardium - innervation</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Vagal nerve</subject><subject>Vagus Nerve - pathology</subject><issn>1054-8807</issn><issn>1879-1336</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkUuPFCEUhYlx4jz0J2hYuqkWKKqgNhrTzqOTGU3Gx5ZQcEtpq6EEapL-91LpHhezcQPcm3PPDd9B6DUlK0po-267MjpOOv9asVKW3oqQ-hk6o1J0Fa3r9nl5k4ZXUhJxis5T2hJCJOf8BTplQjaMEHqG8j3Y2YDFl5MrhtbpEf_QP8v5GeID4E_gk8t7rL3Fm92kXSzag2AdfI5hxM5jje91xnf78Gix8YOOJrvgqxvQMeMr7cY5Ar4LFsaX6GTQY4JXx_sCfb-6_La-qW6_XG_WH28rwxnJlWGd1W3PuGiE7GrdC8bZoKFrhehY0w1UWykMyE7KnsuWtkPfMMGHTtKBkaa-QG8PvlMMf2ZIWe1cMjCO2kOYk6KS04KqEbRIm4PUxJBShEFN0e103CtK1AJcbdURuFqAL-0CvMy9Oa6Y-x3Yf1OPhIvgw0EA5aMPDqJKxoEvyAtKk5UN7r8r3j9xMKPzJa3xN-whbcMcfaGoqEpMEfV1SX0JnbY1oUzy-i_Ha6ge</recordid><startdate>20170101</startdate><enddate>20170101</enddate><creator>Delfiner, Matthew S</creator><creator>Siano, John</creator><creator>Li, Ying</creator><creator>Dedkov, Eduard I</creator><creator>Zhang, Youhua</creator><general>Elsevier Inc</general><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>7X8</scope></search><sort><creationdate>20170101</creationdate><title>Reduced Epicardial Vagal Nerve Density and Impaired Vagal Control in a Rat Myocardial Infarction-Heart Failure Model</title><author>Delfiner, Matthew S ; Siano, John ; Li, Ying ; Dedkov, Eduard I ; Zhang, Youhua</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c420t-c29da6b24757893ab7242fae96779259f1ad87ce8988b48616fb5274f981f2053</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Acetylcholinesterase - analysis</topic><topic>Animals</topic><topic>Autonomic nervous system</topic><topic>Autonomic Nervous System - physiopathology</topic><topic>Disease Models, Animal</topic><topic>Epicardial nerve bundle</topic><topic>Female</topic><topic>Heart failure</topic><topic>Heart Failure - physiopathology</topic><topic>Immunohistochemistry</topic><topic>Male</topic><topic>Myocardial Infarction - physiopathology</topic><topic>Pathology</topic><topic>Pericardium - innervation</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Vagal nerve</topic><topic>Vagus Nerve - pathology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Delfiner, Matthew S</creatorcontrib><creatorcontrib>Siano, John</creatorcontrib><creatorcontrib>Li, Ying</creatorcontrib><creatorcontrib>Dedkov, Eduard I</creatorcontrib><creatorcontrib>Zhang, Youhua</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Cardiovascular pathology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Delfiner, Matthew S</au><au>Siano, John</au><au>Li, Ying</au><au>Dedkov, Eduard I</au><au>Zhang, Youhua</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Reduced Epicardial Vagal Nerve Density and Impaired Vagal Control in a Rat Myocardial Infarction-Heart Failure Model</atitle><jtitle>Cardiovascular pathology</jtitle><addtitle>Cardiovasc Pathol</addtitle><date>2017-01-01</date><risdate>2017</risdate><volume>26</volume><spage>21</spage><epage>29</epage><pages>21-29</pages><issn>1054-8807</issn><eissn>1879-1336</eissn><abstract>Abstract Background Autonomic remodeling, characterized by sympathetic activation and vagal withdrawal, contributes to heart failure (HF) progression. However, the exact mechanism(s) responsible for vagal withdrawal in HF remain(s) unclear, and whether HF causes epicardial autonomic nerve remodeling is unknown. Methods and Results Myocardial infarction (MI) was produced in 14 Sprague–Dawley rats, and 10 sham surgery rats served as the control. MI-HF was confirmed 2 months after the surgery by echocardiography and hemodynamic measurement. Cervical vagal nerve stimulation was delivered to examine the heart rate slowing effect. Whole heart acetylcholinesterase histochemistry was used to examine the epicardial autonomic nerve remodeling at dorsal ventricles (remote from the infarcted area). Compared with the control animals, the same vagal nerve stimulation had less heart rate slowing effect in MI-HF group. Both epicardial nerve bundle length-density (2.56±0.60 μm/mm2 versus 1.68±0.46 μm/mm2 , P =.001) and branching point-density (1.24±0.25 points/mm2 versus 0.66±0.18 points/ mm2 , P <.001) were lower in MI-HF rats. The chemically stained epicardial nerve bundles contain both sympathetic (tyrosine hydroxylase positive) and vagal (choline acetyltransferase positive) fibers. However within the stained nerve bundle, the chemical color corresponds mainly with the vagal fibers. Conclusions Whole heart acetylcholinesterase histochemistry revealed a decreased ventricular epicardial vagal nerve density in MI-HF rats, which may contribute to impaired cardiac vagal control in HF.</abstract><cop>United States</cop><pub>Elsevier Inc</pub><pmid>27852001</pmid><doi>10.1016/j.carpath.2016.10.003</doi><tpages>9</tpages></addata></record> |
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| subjects | Acetylcholinesterase - analysis Animals Autonomic nervous system Autonomic Nervous System - physiopathology Disease Models, Animal Epicardial nerve bundle Female Heart failure Heart Failure - physiopathology Immunohistochemistry Male Myocardial Infarction - physiopathology Pathology Pericardium - innervation Rats Rats, Sprague-Dawley Vagal nerve Vagus Nerve - pathology |
| title | Reduced Epicardial Vagal Nerve Density and Impaired Vagal Control in a Rat Myocardial Infarction-Heart Failure Model |
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