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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Veröffentlicht in:Bioscience reports 2018-06, Vol.38 (3)
Hauptverfasser: 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
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container_issue 3
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container_title Bioscience reports
container_volume 38
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;
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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; &lt;0.05 in each case). 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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; &lt;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 &amp; 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 &amp; 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; &lt;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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