Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation
Cardiac atrophy is the most common complication of prolonged application of the left ventricle (LV) assist device (LVAD) in patients with advanced heart failure (HF). Our aim was to evaluate the course of unloading-induced cardiac atrophy in rats with failing hearts, and to examine if increased isov...
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creator | Pokorný, Martin Mrázová, Iveta Šochman, Jan Melenovský, Vojtěch Malý, Jiří Pirk, Jan Červenková, Lenka Sadowski, Janusz Čermák, Zdeněk Volenec, Karel Vacková, Šárka Maxová, Hana Červenka, Luděk Netuka, Ivan |
description | Cardiac atrophy is the most common complication of prolonged application of the left ventricle (LV) assist device (LVAD) in patients with advanced heart failure (HF). Our aim was to evaluate the course of unloading-induced cardiac atrophy in rats with failing hearts, and to examine if increased isovolumic loading obtained by intraventricular implantation of an especially designed spring expander would attenuate this process. Heterotopic abdominal heart transplantation (HT
) was used as a rat model of heart unloading. HF was induced by volume overload achieved by creation of the aorto-caval fistula (ACF). The degree of cardiac atrophy was assessed as the weight ratio of the heterotopically transplanted heart (HW) to the control heart. Isovolumic loading was increased by intraventricular implantation of a stainless steel three-branch spring expander. The course of cardiac atrophy was evaluated on days 7, 14, 21, and 28 after HT
Seven days unloading by HT
in failing hearts sufficed to substantially decrease the HW (-59 ± 3%), the decrease progressed when measured on days 14, 21, and 28 after HT
Implantation of the spring expander significantly reduced the decreases in whole HW at all the time points (-39 ± 3 compared with -59 ± 3, -52 ± 2 compared with -69 ± 3, -51 ± 2 compared with -71 ± 2, and -44 ± 2 compared with -71 ± 3%, respectively; |
doi_str_mv | 10.1042/BSR20180371 |
format | Article |
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) was used as a rat model of heart unloading. HF was induced by volume overload achieved by creation of the aorto-caval fistula (ACF). The degree of cardiac atrophy was assessed as the weight ratio of the heterotopically transplanted heart (HW) to the control heart. Isovolumic loading was increased by intraventricular implantation of a stainless steel three-branch spring expander. The course of cardiac atrophy was evaluated on days 7, 14, 21, and 28 after HT
Seven days unloading by HT
in failing hearts sufficed to substantially decrease the HW (-59 ± 3%), the decrease progressed when measured on days 14, 21, and 28 after HT
Implantation of the spring expander significantly reduced the decreases in whole HW at all the time points (-39 ± 3 compared with -59 ± 3, -52 ± 2 compared with -69 ± 3, -51 ± 2 compared with -71 ± 2, and -44 ± 2 compared with -71 ± 3%, respectively;
<0.05 in each case). We conclude that the enhanced isovolumic heart loading obtained by implantation of the spring expander attenuates the development of unloading-induced cardiac atrophy in the failing rat heart.</description><identifier>ISSN: 0144-8463</identifier><identifier>EISSN: 1573-4935</identifier><identifier>DOI: 10.1042/BSR20180371</identifier><identifier>PMID: 29743195</identifier><language>eng</language><publisher>England: Portland Press Ltd</publisher><subject>Animals ; Aorta - surgery ; Atrial Natriuretic Factor - genetics ; Atrial Natriuretic Factor - metabolism ; Atrophy - metabolism ; Atrophy - physiopathology ; Atrophy - prevention & control ; Atrophy - surgery ; Biomarkers - metabolism ; Disease Models, Animal ; Equipment Design ; Fibroblast Growth Factor 2 - genetics ; Fibroblast Growth Factor 2 - metabolism ; Fistula ; Gene Expression ; Glucose Transporter Type 1 - genetics ; Glucose Transporter Type 1 - metabolism ; Heart - physiopathology ; Heart Failure - metabolism ; Heart Failure - physiopathology ; Heart Failure - surgery ; Heart Failure - therapy ; Heart Transplantation ; Heart Ventricles - physiopathology ; Heart Ventricles - surgery ; Humans ; Implants, Experimental ; Male ; Rats ; Rats, Inbred Lew ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics ; Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism ; Tissue Expansion Devices ; Transplantation, Heterotopic ; Vena Cava, Superior - surgery</subject><ispartof>Bioscience reports, 2018-06, Vol.38 (3)</ispartof><rights>2018 The Author(s).</rights><rights>2018 The Author(s). 2018</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c381t-4407ebf93054578164fb719a1982208936c91d7e89a1eaad57b0af98a197f24f3</citedby><cites>FETCH-LOGICAL-c381t-4407ebf93054578164fb719a1982208936c91d7e89a1eaad57b0af98a197f24f3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6019382/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC6019382/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,27903,27904,33432,33510,33683,33724,33985,34294,34314,36245,53770,53772,64364</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/29743195$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Pokorný, Martin</creatorcontrib><creatorcontrib>Mrázová, Iveta</creatorcontrib><creatorcontrib>Šochman, Jan</creatorcontrib><creatorcontrib>Melenovský, Vojtěch</creatorcontrib><creatorcontrib>Malý, Jiří</creatorcontrib><creatorcontrib>Pirk, Jan</creatorcontrib><creatorcontrib>Červenková, Lenka</creatorcontrib><creatorcontrib>Sadowski, Janusz</creatorcontrib><creatorcontrib>Čermák, Zdeněk</creatorcontrib><creatorcontrib>Volenec, Karel</creatorcontrib><creatorcontrib>Vacková, Šárka</creatorcontrib><creatorcontrib>Maxová, Hana</creatorcontrib><creatorcontrib>Červenka, Luděk</creatorcontrib><creatorcontrib>Netuka, Ivan</creatorcontrib><title>Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation</title><title>Bioscience reports</title><addtitle>Biosci Rep</addtitle><description>Cardiac atrophy is the most common complication of prolonged application of the left ventricle (LV) assist device (LVAD) in patients with advanced heart failure (HF). Our aim was to evaluate the course of unloading-induced cardiac atrophy in rats with failing hearts, and to examine if increased isovolumic loading obtained by intraventricular implantation of an especially designed spring expander would attenuate this process. Heterotopic abdominal heart transplantation (HT
) was used as a rat model of heart unloading. HF was induced by volume overload achieved by creation of the aorto-caval fistula (ACF). The degree of cardiac atrophy was assessed as the weight ratio of the heterotopically transplanted heart (HW) to the control heart. Isovolumic loading was increased by intraventricular implantation of a stainless steel three-branch spring expander. The course of cardiac atrophy was evaluated on days 7, 14, 21, and 28 after HT
Seven days unloading by HT
in failing hearts sufficed to substantially decrease the HW (-59 ± 3%), the decrease progressed when measured on days 14, 21, and 28 after HT
Implantation of the spring expander significantly reduced the decreases in whole HW at all the time points (-39 ± 3 compared with -59 ± 3, -52 ± 2 compared with -69 ± 3, -51 ± 2 compared with -71 ± 2, and -44 ± 2 compared with -71 ± 3%, respectively;
<0.05 in each case). We conclude that the enhanced isovolumic heart loading obtained by implantation of the spring expander attenuates the development of unloading-induced cardiac atrophy in the failing rat heart.</description><subject>Animals</subject><subject>Aorta - surgery</subject><subject>Atrial Natriuretic Factor - genetics</subject><subject>Atrial Natriuretic Factor - metabolism</subject><subject>Atrophy - metabolism</subject><subject>Atrophy - physiopathology</subject><subject>Atrophy - prevention & control</subject><subject>Atrophy - surgery</subject><subject>Biomarkers - metabolism</subject><subject>Disease Models, Animal</subject><subject>Equipment Design</subject><subject>Fibroblast Growth Factor 2 - genetics</subject><subject>Fibroblast Growth Factor 2 - metabolism</subject><subject>Fistula</subject><subject>Gene Expression</subject><subject>Glucose Transporter Type 1 - genetics</subject><subject>Glucose Transporter Type 1 - metabolism</subject><subject>Heart - physiopathology</subject><subject>Heart Failure - metabolism</subject><subject>Heart Failure - physiopathology</subject><subject>Heart Failure - surgery</subject><subject>Heart Failure - therapy</subject><subject>Heart Transplantation</subject><subject>Heart Ventricles - physiopathology</subject><subject>Heart Ventricles - surgery</subject><subject>Humans</subject><subject>Implants, Experimental</subject><subject>Male</subject><subject>Rats</subject><subject>Rats, Inbred Lew</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics</subject><subject>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</subject><subject>Tissue Expansion Devices</subject><subject>Transplantation, Heterotopic</subject><subject>Vena Cava, Superior - surgery</subject><issn>0144-8463</issn><issn>1573-4935</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2018</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpVkU9vFSEUxYnR2Nfqyr1hadKMhYEZYGOiTa1Nmpj4Z03uMNDBzAwjMC--D-N3lcmrTbu5hHt_nMPNQegNJe8p4fXFp-_fakIlYYI-QzvaCFZxxZrnaEco55XkLTtBpyn9IoSUAX-JTmolOKOq2aG_Nynsw7hO3uAxQO_nOxwczoPFDvy4XQcLMePugP2cI-xtqd6sI0S8jGDsVBrbE8BpiRtv_yww9zZiyNnOK2SbsIHYezClFcMyHDC4XIDBlhpyWIr50aUYzKnIzhmyD_Mr9MLBmOzr-_MM_fx89ePyS3X79frm8uNtZZikueKcCNs5xUjDGyFpy10nqAKqZF0TqVhrFO2FlaVlAfpGdASckgUQruaOnaEPR91l7Sbbm21HGHXZZ4J40AG8fjqZ_aDvwl63hCom6yLw7l4ght-rTVlPPhk7lk1sWJOuSzqkpUypgp4fURNDStG6BxtK9BaofhRood8-_tkD-z9B9g-R-aCN</recordid><startdate>20180629</startdate><enddate>20180629</enddate><creator>Pokorný, Martin</creator><creator>Mrázová, Iveta</creator><creator>Šochman, Jan</creator><creator>Melenovský, Vojtěch</creator><creator>Malý, Jiří</creator><creator>Pirk, Jan</creator><creator>Červenková, Lenka</creator><creator>Sadowski, Janusz</creator><creator>Čermák, Zdeněk</creator><creator>Volenec, Karel</creator><creator>Vacková, Šárka</creator><creator>Maxová, Hana</creator><creator>Červenka, Luděk</creator><creator>Netuka, Ivan</creator><general>Portland Press Ltd</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><scope>5PM</scope></search><sort><creationdate>20180629</creationdate><title>Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation</title><author>Pokorný, Martin ; Mrázová, Iveta ; Šochman, Jan ; Melenovský, Vojtěch ; Malý, Jiří ; Pirk, Jan ; Červenková, Lenka ; Sadowski, Janusz ; Čermák, Zdeněk ; Volenec, Karel ; Vacková, Šárka ; Maxová, Hana ; Červenka, Luděk ; Netuka, Ivan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c381t-4407ebf93054578164fb719a1982208936c91d7e89a1eaad57b0af98a197f24f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2018</creationdate><topic>Animals</topic><topic>Aorta - surgery</topic><topic>Atrial Natriuretic Factor - genetics</topic><topic>Atrial Natriuretic Factor - metabolism</topic><topic>Atrophy - metabolism</topic><topic>Atrophy - physiopathology</topic><topic>Atrophy - prevention & control</topic><topic>Atrophy - surgery</topic><topic>Biomarkers - metabolism</topic><topic>Disease Models, Animal</topic><topic>Equipment Design</topic><topic>Fibroblast Growth Factor 2 - genetics</topic><topic>Fibroblast Growth Factor 2 - metabolism</topic><topic>Fistula</topic><topic>Gene Expression</topic><topic>Glucose Transporter Type 1 - genetics</topic><topic>Glucose Transporter Type 1 - metabolism</topic><topic>Heart - physiopathology</topic><topic>Heart Failure - metabolism</topic><topic>Heart Failure - physiopathology</topic><topic>Heart Failure - surgery</topic><topic>Heart Failure - therapy</topic><topic>Heart Transplantation</topic><topic>Heart Ventricles - physiopathology</topic><topic>Heart Ventricles - surgery</topic><topic>Humans</topic><topic>Implants, Experimental</topic><topic>Male</topic><topic>Rats</topic><topic>Rats, Inbred Lew</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics</topic><topic>Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism</topic><topic>Tissue Expansion Devices</topic><topic>Transplantation, Heterotopic</topic><topic>Vena Cava, Superior - surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pokorný, Martin</creatorcontrib><creatorcontrib>Mrázová, Iveta</creatorcontrib><creatorcontrib>Šochman, Jan</creatorcontrib><creatorcontrib>Melenovský, Vojtěch</creatorcontrib><creatorcontrib>Malý, Jiří</creatorcontrib><creatorcontrib>Pirk, Jan</creatorcontrib><creatorcontrib>Červenková, Lenka</creatorcontrib><creatorcontrib>Sadowski, Janusz</creatorcontrib><creatorcontrib>Čermák, Zdeněk</creatorcontrib><creatorcontrib>Volenec, Karel</creatorcontrib><creatorcontrib>Vacková, Šárka</creatorcontrib><creatorcontrib>Maxová, Hana</creatorcontrib><creatorcontrib>Červenka, Luděk</creatorcontrib><creatorcontrib>Netuka, Ivan</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><collection>PubMed Central (Full Participant titles)</collection><jtitle>Bioscience reports</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Pokorný, Martin</au><au>Mrázová, Iveta</au><au>Šochman, Jan</au><au>Melenovský, Vojtěch</au><au>Malý, Jiří</au><au>Pirk, Jan</au><au>Červenková, Lenka</au><au>Sadowski, Janusz</au><au>Čermák, Zdeněk</au><au>Volenec, Karel</au><au>Vacková, Šárka</au><au>Maxová, Hana</au><au>Červenka, Luděk</au><au>Netuka, Ivan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation</atitle><jtitle>Bioscience reports</jtitle><addtitle>Biosci Rep</addtitle><date>2018-06-29</date><risdate>2018</risdate><volume>38</volume><issue>3</issue><issn>0144-8463</issn><eissn>1573-4935</eissn><abstract>Cardiac atrophy is the most common complication of prolonged application of the left ventricle (LV) assist device (LVAD) in patients with advanced heart failure (HF). Our aim was to evaluate the course of unloading-induced cardiac atrophy in rats with failing hearts, and to examine if increased isovolumic loading obtained by intraventricular implantation of an especially designed spring expander would attenuate this process. Heterotopic abdominal heart transplantation (HT
) was used as a rat model of heart unloading. HF was induced by volume overload achieved by creation of the aorto-caval fistula (ACF). The degree of cardiac atrophy was assessed as the weight ratio of the heterotopically transplanted heart (HW) to the control heart. Isovolumic loading was increased by intraventricular implantation of a stainless steel three-branch spring expander. The course of cardiac atrophy was evaluated on days 7, 14, 21, and 28 after HT
Seven days unloading by HT
in failing hearts sufficed to substantially decrease the HW (-59 ± 3%), the decrease progressed when measured on days 14, 21, and 28 after HT
Implantation of the spring expander significantly reduced the decreases in whole HW at all the time points (-39 ± 3 compared with -59 ± 3, -52 ± 2 compared with -69 ± 3, -51 ± 2 compared with -71 ± 2, and -44 ± 2 compared with -71 ± 3%, respectively;
<0.05 in each case). We conclude that the enhanced isovolumic heart loading obtained by implantation of the spring expander attenuates the development of unloading-induced cardiac atrophy in the failing rat heart.</abstract><cop>England</cop><pub>Portland Press Ltd</pub><pmid>29743195</pmid><doi>10.1042/BSR20180371</doi><oa>free_for_read</oa></addata></record> |
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subjects | Animals Aorta - surgery Atrial Natriuretic Factor - genetics Atrial Natriuretic Factor - metabolism Atrophy - metabolism Atrophy - physiopathology Atrophy - prevention & control Atrophy - surgery Biomarkers - metabolism Disease Models, Animal Equipment Design Fibroblast Growth Factor 2 - genetics Fibroblast Growth Factor 2 - metabolism Fistula Gene Expression Glucose Transporter Type 1 - genetics Glucose Transporter Type 1 - metabolism Heart - physiopathology Heart Failure - metabolism Heart Failure - physiopathology Heart Failure - surgery Heart Failure - therapy Heart Transplantation Heart Ventricles - physiopathology Heart Ventricles - surgery Humans Implants, Experimental Male Rats Rats, Inbred Lew Sarcoplasmic Reticulum Calcium-Transporting ATPases - genetics Sarcoplasmic Reticulum Calcium-Transporting ATPases - metabolism Tissue Expansion Devices Transplantation, Heterotopic Vena Cava, Superior - surgery |
title | Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation |
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