Development of a Rat Model of Sick Sinus Syndrome Using Pinpoint Press Permeation
Objective. Sick sinus syndrome (SSS) is one of the most common causes of cardiac impairment necessitating pacemaker implantation. However, studies of SSS pathogenesis are neither comprehensive nor conclusive due to limited success in achieving a stable rat SSS model. Here, we modified pinpoint press...
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| description | Objective. Sick sinus syndrome (SSS) is one of the most common causes of cardiac impairment necessitating pacemaker implantation. However, studies of SSS pathogenesis are neither comprehensive nor conclusive due to limited success in achieving a stable rat SSS model. Here, we modified pinpoint press permeation to establish a stable rat SSS model. Methods. We randomly assigned 138 male Sprague-Dawley rats into three groups: normal control (n = 8), sham (n = 10), and SSS (n = 120). Postoperatively, the SSS group was further divided into SSSA (n = 40), SSSB (n = 40), and SSSC (n = 40), based on reduction in heart rates by 20–30%, 31–40%, and 41–50%, respectively. We also assessed histomorphological characteristics and hyperpolarization-activated cyclic nucleotide-gated cation channel 4 (HCN4) expression in the sinoatrial node (SAN) at 1, 2, 3, and 4 weeks after surgery. Results. Mortality was statistically higher in SSSC compared to SSSA and SSSB (7.5% versus 90.0% and 87.5%; P < 0.05). Heart rate in SSSA was gradually restored to preoperative levels by week 4 after surgery. In contrast, heart rate in SSSB was stable at 2–3 weeks after surgery. However, we observed that the tissues and cells in SAN were severely injured and also found a time-dependent increase in collagen content and atrium myocardium in SSSB. HCN4 expression was significantly reduced at all 4 time points in SSSB, with statistically significant differences among the groups (P < 0.01). Conclusion. We successfully developed a rat SSS model that was sustainable for up to 4 weeks. |
| doi_str_mv | 10.1155/2018/7487324 |
| format | Article |
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Sick sinus syndrome (SSS) is one of the most common causes of cardiac impairment necessitating pacemaker implantation. However, studies of SSS pathogenesis are neither comprehensive nor conclusive due to limited success in achieving a stable rat SSS model. Here, we modified pinpoint press permeation to establish a stable rat SSS model. Methods. We randomly assigned 138 male Sprague-Dawley rats into three groups: normal control (n = 8), sham (n = 10), and SSS (n = 120). Postoperatively, the SSS group was further divided into SSSA (n = 40), SSSB (n = 40), and SSSC (n = 40), based on reduction in heart rates by 20–30%, 31–40%, and 41–50%, respectively. We also assessed histomorphological characteristics and hyperpolarization-activated cyclic nucleotide-gated cation channel 4 (HCN4) expression in the sinoatrial node (SAN) at 1, 2, 3, and 4 weeks after surgery. Results. Mortality was statistically higher in SSSC compared to SSSA and SSSB (7.5% versus 90.0% and 87.5%; P < 0.05). Heart rate in SSSA was gradually restored to preoperative levels by week 4 after surgery. In contrast, heart rate in SSSB was stable at 2–3 weeks after surgery. However, we observed that the tissues and cells in SAN were severely injured and also found a time-dependent increase in collagen content and atrium myocardium in SSSB. HCN4 expression was significantly reduced at all 4 time points in SSSB, with statistically significant differences among the groups (P < 0.01). Conclusion. We successfully developed a rat SSS model that was sustainable for up to 4 weeks.</description><identifier>ISSN: 2314-6133</identifier><identifier>EISSN: 2314-6141</identifier><identifier>DOI: 10.1155/2018/7487324</identifier><identifier>PMID: 30581867</identifier><language>eng</language><publisher>Cairo, Egypt: Hindawi Publishing Corporation</publisher><subject>Animals ; Atrium ; Cardiac arrhythmia ; Caustic soda ; Collagen ; Cotton ; Disease Models, Animal ; Heart Atria - metabolism ; Heart Atria - physiopathology ; Heart beat ; Heart rate ; Heart Rate - physiology ; Hyperpolarization ; Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism ; Hypertension ; Implantation ; Ion channels ; Ion channels (cyclic nucleotide-gated) ; Laboratory animals ; Male ; Methods ; Myocardium ; Ostomy ; Pathogenesis ; Penetration ; Physiology ; Rats ; Rats, Sprague-Dawley ; Rodents ; Sick sinus syndrome ; Sick Sinus Syndrome - metabolism ; Sick Sinus Syndrome - physiopathology ; Signal transduction ; Sinoatrial Node - metabolism ; Sinoatrial Node - physiopathology ; Sinuses ; Sodium ; Statistical analysis ; Studies ; Success ; Surgery ; Time dependence ; Ventilators</subject><ispartof>BioMed research international, 2018-01, Vol.2018 (2018), p.1-7</ispartof><rights>Copyright © 2018 Hong-bin Zhong et al.</rights><rights>COPYRIGHT 2018 John Wiley & Sons, Inc.</rights><rights>Copyright © 2018 Hong-bin Zhong et al. This is an open access article distributed under the Creative Commons Attribution License (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License. https://creativecommons.org/licenses/by/4.0</rights><rights>Copyright © 2018 Hong-bin Zhong et al. 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c499t-f152bdf3eff53ed463972966c09ce6c953b00710a3ab5aa588f0a8eb5c381b783</citedby><cites>FETCH-LOGICAL-c499t-f152bdf3eff53ed463972966c09ce6c953b00710a3ab5aa588f0a8eb5c381b783</cites><orcidid>0000-0003-0945-5514</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6276488/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6276488/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,315,728,781,785,886,27928,27929,53795,53797</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/30581867$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Mariscalco, Giovanni</contributor><contributor>Giovanni Mariscalco</contributor><creatorcontrib>Wang, Hua-jun</creatorcontrib><creatorcontrib>Xu, Chang-Sheng</creatorcontrib><creatorcontrib>Lian, Gui-li</creatorcontrib><creatorcontrib>Wang, Ting-jun</creatorcontrib><creatorcontrib>Zhong, Hong-bin</creatorcontrib><creatorcontrib>Xie, Liangdi</creatorcontrib><title>Development of a Rat Model of Sick Sinus Syndrome Using Pinpoint Press Permeation</title><title>BioMed research international</title><addtitle>Biomed Res Int</addtitle><description>Objective. Sick sinus syndrome (SSS) is one of the most common causes of cardiac impairment necessitating pacemaker implantation. However, studies of SSS pathogenesis are neither comprehensive nor conclusive due to limited success in achieving a stable rat SSS model. Here, we modified pinpoint press permeation to establish a stable rat SSS model. Methods. We randomly assigned 138 male Sprague-Dawley rats into three groups: normal control (n = 8), sham (n = 10), and SSS (n = 120). Postoperatively, the SSS group was further divided into SSSA (n = 40), SSSB (n = 40), and SSSC (n = 40), based on reduction in heart rates by 20–30%, 31–40%, and 41–50%, respectively. We also assessed histomorphological characteristics and hyperpolarization-activated cyclic nucleotide-gated cation channel 4 (HCN4) expression in the sinoatrial node (SAN) at 1, 2, 3, and 4 weeks after surgery. Results. Mortality was statistically higher in SSSC compared to SSSA and SSSB (7.5% versus 90.0% and 87.5%; P < 0.05). Heart rate in SSSA was gradually restored to preoperative levels by week 4 after surgery. In contrast, heart rate in SSSB was stable at 2–3 weeks after surgery. However, we observed that the tissues and cells in SAN were severely injured and also found a time-dependent increase in collagen content and atrium myocardium in SSSB. HCN4 expression was significantly reduced at all 4 time points in SSSB, with statistically significant differences among the groups (P < 0.01). Conclusion. We successfully developed a rat SSS model that was sustainable for up to 4 weeks.</description><subject>Animals</subject><subject>Atrium</subject><subject>Cardiac arrhythmia</subject><subject>Caustic soda</subject><subject>Collagen</subject><subject>Cotton</subject><subject>Disease Models, Animal</subject><subject>Heart Atria - metabolism</subject><subject>Heart Atria - physiopathology</subject><subject>Heart beat</subject><subject>Heart rate</subject><subject>Heart Rate - physiology</subject><subject>Hyperpolarization</subject><subject>Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism</subject><subject>Hypertension</subject><subject>Implantation</subject><subject>Ion channels</subject><subject>Ion channels (cyclic nucleotide-gated)</subject><subject>Laboratory animals</subject><subject>Male</subject><subject>Methods</subject><subject>Myocardium</subject><subject>Ostomy</subject><subject>Pathogenesis</subject><subject>Penetration</subject><subject>Physiology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Rodents</subject><subject>Sick sinus syndrome</subject><subject>Sick Sinus Syndrome - metabolism</subject><subject>Sick Sinus Syndrome - physiopathology</subject><subject>Signal transduction</subject><subject>Sinoatrial Node - metabolism</subject><subject>Sinoatrial Node - physiopathology</subject><subject>Sinuses</subject><subject>Sodium</subject><subject>Statistical analysis</subject><subject>Studies</subject><subject>Success</subject><subject>Surgery</subject><subject>Time dependence</subject><subject>Ventilators</subject><issn>2314-6133</issn><issn>2314-6141</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>RHX</sourceid><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><recordid>eNqNkUtv1DAUhS0EolXpjjWKxAYJhvodZ4NUlUcrtWKgdG05zvXUJbGndlLUf4-jGabQFV74IX_3-B4fhF4S_J4QIY4oJuqo5qpmlD9B-5QRvpCEk6e7PWN76DDnG1yGIhI38jnaY1goomS9j759hDvo43qAMFbRVab6bsbqInbQz8dLb3-WKUy5urwPXYoDVFfZh1W19GEdfSlaJsi5WkIawIw-hhfomTN9hsPteoCuPn_6cXK6OP_65ezk-HxhedOMC0cEbTvHwDnBoOOSNTVtpLS4sSBtI1iLcU2wYaYVxgilHDYKWmGZIm2t2AH6sNFdT-0AnS0Gkun1OvnBpHsdjdf_3gR_rVfxTktaS65mgTdbgRRvJ8ijHny20PcmQJyypuW3iGC1aAr6-hF6E6cUir1CcaxYaVU8UCvTg_bBxfKunUX1saSkbpTCtFDvNpRNMecEbtcywXoOVc-h6m2oBX_1t80d_CfCArzdANc-dOaX_085KAw480ATqgRX7Dfpx7Fm</recordid><startdate>20180101</startdate><enddate>20180101</enddate><creator>Wang, Hua-jun</creator><creator>Xu, Chang-Sheng</creator><creator>Lian, Gui-li</creator><creator>Wang, Ting-jun</creator><creator>Zhong, Hong-bin</creator><creator>Xie, Liangdi</creator><general>Hindawi Publishing Corporation</general><general>Hindawi</general><general>John Wiley & Sons, Inc</general><general>Hindawi Limited</general><scope>ADJCN</scope><scope>AHFXO</scope><scope>RHU</scope><scope>RHW</scope><scope>RHX</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>7QL</scope><scope>7QO</scope><scope>7T7</scope><scope>7TK</scope><scope>7U7</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>CWDGH</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>LK8</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope><orcidid>https://orcid.org/0000-0003-0945-5514</orcidid></search><sort><creationdate>20180101</creationdate><title>Development of a Rat Model of Sick Sinus Syndrome Using Pinpoint Press Permeation</title><author>Wang, Hua-jun ; Xu, Chang-Sheng ; Lian, Gui-li ; Wang, Ting-jun ; Zhong, Hong-bin ; Xie, Liangdi</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c499t-f152bdf3eff53ed463972966c09ce6c953b00710a3ab5aa588f0a8eb5c381b783</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Atrium</topic><topic>Cardiac arrhythmia</topic><topic>Caustic soda</topic><topic>Collagen</topic><topic>Cotton</topic><topic>Disease Models, Animal</topic><topic>Heart Atria - metabolism</topic><topic>Heart Atria - physiopathology</topic><topic>Heart beat</topic><topic>Heart rate</topic><topic>Heart Rate - physiology</topic><topic>Hyperpolarization</topic><topic>Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism</topic><topic>Hypertension</topic><topic>Implantation</topic><topic>Ion channels</topic><topic>Ion channels (cyclic nucleotide-gated)</topic><topic>Laboratory animals</topic><topic>Male</topic><topic>Methods</topic><topic>Myocardium</topic><topic>Ostomy</topic><topic>Pathogenesis</topic><topic>Penetration</topic><topic>Physiology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Rodents</topic><topic>Sick sinus syndrome</topic><topic>Sick Sinus Syndrome - metabolism</topic><topic>Sick Sinus Syndrome - physiopathology</topic><topic>Signal transduction</topic><topic>Sinoatrial Node - metabolism</topic><topic>Sinoatrial Node - physiopathology</topic><topic>Sinuses</topic><topic>Sodium</topic><topic>Statistical analysis</topic><topic>Studies</topic><topic>Success</topic><topic>Surgery</topic><topic>Time dependence</topic><topic>Ventilators</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Wang, Hua-jun</creatorcontrib><creatorcontrib>Xu, Chang-Sheng</creatorcontrib><creatorcontrib>Lian, Gui-li</creatorcontrib><creatorcontrib>Wang, Ting-jun</creatorcontrib><creatorcontrib>Zhong, Hong-bin</creatorcontrib><creatorcontrib>Xie, Liangdi</creatorcontrib><collection>الدوريات العلمية والإحصائية - 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Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>BioMed research international</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wang, Hua-jun</au><au>Xu, Chang-Sheng</au><au>Lian, Gui-li</au><au>Wang, Ting-jun</au><au>Zhong, Hong-bin</au><au>Xie, Liangdi</au><au>Mariscalco, Giovanni</au><au>Giovanni Mariscalco</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Development of a Rat Model of Sick Sinus Syndrome Using Pinpoint Press Permeation</atitle><jtitle>BioMed research international</jtitle><addtitle>Biomed Res Int</addtitle><date>2018-01-01</date><risdate>2018</risdate><volume>2018</volume><issue>2018</issue><spage>1</spage><epage>7</epage><pages>1-7</pages><issn>2314-6133</issn><eissn>2314-6141</eissn><abstract>Objective. Sick sinus syndrome (SSS) is one of the most common causes of cardiac impairment necessitating pacemaker implantation. However, studies of SSS pathogenesis are neither comprehensive nor conclusive due to limited success in achieving a stable rat SSS model. Here, we modified pinpoint press permeation to establish a stable rat SSS model. Methods. We randomly assigned 138 male Sprague-Dawley rats into three groups: normal control (n = 8), sham (n = 10), and SSS (n = 120). Postoperatively, the SSS group was further divided into SSSA (n = 40), SSSB (n = 40), and SSSC (n = 40), based on reduction in heart rates by 20–30%, 31–40%, and 41–50%, respectively. We also assessed histomorphological characteristics and hyperpolarization-activated cyclic nucleotide-gated cation channel 4 (HCN4) expression in the sinoatrial node (SAN) at 1, 2, 3, and 4 weeks after surgery. Results. Mortality was statistically higher in SSSC compared to SSSA and SSSB (7.5% versus 90.0% and 87.5%; P < 0.05). Heart rate in SSSA was gradually restored to preoperative levels by week 4 after surgery. In contrast, heart rate in SSSB was stable at 2–3 weeks after surgery. However, we observed that the tissues and cells in SAN were severely injured and also found a time-dependent increase in collagen content and atrium myocardium in SSSB. HCN4 expression was significantly reduced at all 4 time points in SSSB, with statistically significant differences among the groups (P < 0.01). Conclusion. We successfully developed a rat SSS model that was sustainable for up to 4 weeks.</abstract><cop>Cairo, Egypt</cop><pub>Hindawi Publishing Corporation</pub><pmid>30581867</pmid><doi>10.1155/2018/7487324</doi><tpages>7</tpages><orcidid>https://orcid.org/0000-0003-0945-5514</orcidid><oa>free_for_read</oa></addata></record> |
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| subjects | Animals Atrium Cardiac arrhythmia Caustic soda Collagen Cotton Disease Models, Animal Heart Atria - metabolism Heart Atria - physiopathology Heart beat Heart rate Heart Rate - physiology Hyperpolarization Hyperpolarization-Activated Cyclic Nucleotide-Gated Channels - metabolism Hypertension Implantation Ion channels Ion channels (cyclic nucleotide-gated) Laboratory animals Male Methods Myocardium Ostomy Pathogenesis Penetration Physiology Rats Rats, Sprague-Dawley Rodents Sick sinus syndrome Sick Sinus Syndrome - metabolism Sick Sinus Syndrome - physiopathology Signal transduction Sinoatrial Node - metabolism Sinoatrial Node - physiopathology Sinuses Sodium Statistical analysis Studies Success Surgery Time dependence Ventilators |
| title | Development of a Rat Model of Sick Sinus Syndrome Using Pinpoint Press Permeation |
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