Detail
Article
Online article
FT
Medvik - BMC
  • Something wrong with this record ?

Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation

M. Pokorný, I. Mrázová, J. Šochman, V. Melenovský, J. Malý, J. Pirk, L. Červenková, J. Sadowski, Z. Čermák, K. Volenec, Š. Vacková, H. Maxová, L. Červenka, I. Netuka,

. 2018 ; 38 (3) : . [pub] 20180627

Language English Country England, Great Britain

Document type Journal Article, Research Support, Non-U.S. Gov't

Persistent link   https://www.medvik.cz/link/bmc19012680

Grant support
NV16-27420A MZ0 CEP Register

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 (HTx) 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 HTx Seven days unloading by HTx in failing hearts sufficed to substantially decrease the HW (-59 ± 3%), the decrease progressed when measured on days 14, 21, and 28 after HTx 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; P<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.

References provided by Crossref.org

000      
00000naa a2200000 a 4500
001      
bmc19012680
003      
CZ-PrNML
005      
20191220084833.0
007      
ta
008      
190405s2018 enk f 000 0|eng||
009      
AR
024    7_
$a 10.1042/BSR20180371 $2 doi
035    __
$a (PubMed)29743195
040    __
$a ABA008 $b cze $d ABA008 $e AACR2
041    0_
$a eng
044    __
$a enk
100    1_
$a Pokorný, Martin $u Department of Cardiovascular Surgery, Institute for Clinical and Experimental Medicine, Prague, Czech Republic. Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic.
245    10
$a Isovolumic loading of the failing heart by intraventricular placement of a spring expander attenuates cardiac atrophy after heterotopic heart transplantation / $c M. Pokorný, I. Mrázová, J. Šochman, V. Melenovský, J. Malý, J. Pirk, L. Červenková, J. Sadowski, Z. Čermák, K. Volenec, Š. Vacková, H. Maxová, L. Červenka, I. Netuka,
520    9_
$a 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 (HTx) 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 HTx Seven days unloading by HTx in failing hearts sufficed to substantially decrease the HW (-59 ± 3%), the decrease progressed when measured on days 14, 21, and 28 after HTx 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; P<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.
650    _2
$a zvířata $7 D000818
650    _2
$a aorta $x chirurgie $7 D001011
650    _2
$a atriální natriuretický faktor $x genetika $x metabolismus $7 D009320
650    _2
$a atrofie $x metabolismus $x patofyziologie $x prevence a kontrola $x chirurgie $7 D001284
650    _2
$a biologické markery $x metabolismus $7 D015415
650    _2
$a modely nemocí na zvířatech $7 D004195
650    _2
$a design vybavení $7 D004867
650    _2
$a fibroblastový růstový faktor 2 $x genetika $x metabolismus $7 D016222
650    _2
$a píštěle $7 D005402
650    _2
$a exprese genu $7 D015870
650    _2
$a přenašeč glukosy typ 1 $x genetika $x metabolismus $7 D051272
650    _2
$a srdce $x patofyziologie $7 D006321
650    _2
$a srdeční selhání $x metabolismus $x patofyziologie $x chirurgie $x terapie $7 D006333
650    12
$a transplantace srdce $7 D016027
650    _2
$a srdeční komory $x patofyziologie $x chirurgie $7 D006352
650    _2
$a lidé $7 D006801
650    _2
$a experimentální implantáty $7 D020007
650    _2
$a mužské pohlaví $7 D008297
650    _2
$a krysa rodu Rattus $7 D051381
650    _2
$a potkani inbrední LEW $7 D011917
650    _2
$a sarkoplazmatická Ca2+-ATPáza $x genetika $x metabolismus $7 D053498
650    12
$a tkáňové expandéry $7 D015625
650    _2
$a heterotopická transplantace $7 D016042
650    _2
$a vena cava superior $x chirurgie $7 D014683
655    _2
$a časopisecké články $7 D016428
655    _2
$a práce podpořená grantem $7 D013485
700    1_
$a Mrázová, Iveta $u Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic. Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Šochman, Jan, $d 1956- $7 xx0088500 $u Department of Cardiology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Melenovský, Vojtěch $u Department of Cardiology, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Malý, Jiří $u Department of Cardiovascular Surgery, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Pirk, Jan $u Department of Cardiovascular Surgery, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Červenková, Lenka $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Sadowski, Janusz $u Department of Renal and Body Fluid Physiology, Mossakowski Medical Research Centre, Polish Academy of Sciences, Warsaw, Poland.
700    1_
$a Čermák, Zdeněk $u ELLA-CS, Ltd., Hradec Králové, Czech Republic.
700    1_
$a Volenec, Karel $u ELLA-CS, Ltd., Hradec Králové, Czech Republic.
700    1_
$a Vacková, Šárka $u Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Maxová, Hana $u Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic.
700    1_
$a Červenka, Luděk $u Department of Pathophysiology, Second Faculty of Medicine, Charles University, Prague, Czech Republic luce@medicon.cz. Center for Experimental Medicine, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
700    1_
$a Netuka, Ivan $u Department of Cardiovascular Surgery, Institute for Clinical and Experimental Medicine, Prague, Czech Republic.
773    0_
$w MED00000783 $t Bioscience reports $x 1573-4935 $g Roč. 38, č. 3 (2018)
856    41
$u https://pubmed.ncbi.nlm.nih.gov/29743195 $y Pubmed
910    __
$a ABA008 $b sig $c sign $y a $z 0
990    __
$a 20190405 $b ABA008
991    __
$a 20191220085141 $b ABA008
999    __
$a ok $b bmc $g 1391990 $s 1050985
BAS    __
$a 3
BAS    __
$a PreBMC
BMC    __
$a 2018 $b 38 $c 3 $e 20180627 $i 1573-4935 $m Bioscience reports $n Biosci Rep $x MED00000783
GRA    __
$a NV16-27420A $p MZ0
LZP    __
$a Pubmed-20190405

Find record

Citation metrics

Archiving options