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.

• Klíčová slova
• Cardiac atrophy, heart failure, heterotopic heart transplantation, mechanical heart unloading, spring expander,
• MeSH
• aorta chirurgie   MeSH
• atriální natriuretický faktor genetika   metabolismus   MeSH
• atrofie metabolismus   patofyziologie   prevence a kontrola   chirurgie   MeSH
• biologické markery metabolismus   MeSH
• design vybavení MeSH
• experimentální implantáty MeSH
• exprese genu MeSH
• fibroblastový růstový faktor 2 genetika   metabolismus   MeSH
• heterotopická transplantace MeSH
• krysa rodu Rattus MeSH
• lidé MeSH
• modely nemocí na zvířatech MeSH
• píštěle MeSH
• potkani inbrední LEW MeSH
• přenašeč glukosy typ 1 genetika   metabolismus   MeSH
• sarkoplazmatická Ca2+-ATPáza genetika   metabolismus   MeSH
• srdce patofyziologie   MeSH
• srdeční komory patofyziologie   chirurgie   MeSH
• srdeční selhání metabolismus   patofyziologie   chirurgie   terapie   MeSH
• tkáňové expandéry * MeSH
• transplantace srdce * MeSH
• vena cava superior chirurgie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu Rattus MeSH
• lidé MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• Názvy látek
• Atp2a1 protein, rat MeSH Prohlížeč
• atriální natriuretický faktor MeSH
• biologické markery MeSH
• fibroblastový růstový faktor 2 MeSH
• přenašeč glukosy typ 1 MeSH
• sarkoplazmatická Ca2+-ATPáza MeSH
• Slc2a1 protein, rat MeSH Prohlížeč

Genetic polymorphisms of factors regulating the function of endothelium and blood pressure are recently intensively studied also in type 2 diabetes because endothelial dysfunction and arterial hypertension are risk factors of atherosclerosis. The following review deals with relations of polymorphisms in the renin-angiotensin-aldosterone (RAAS) system, polymorphisms of NO-synthase (NOS) as well as the gene for atrial natriuretic peptide (hANP). So far most information was assembled on the influence of polymorphisms of RAAS genes, in particular the gene coding the angiotensin converting enzyme (ACE), on complications of type 2 diabetes. A relationship with the development of coronary disease was described in ACE genes, the receptor for angiotensin II--type 1 (AT1R), angiotensinogen and in several NOS polymorphisms. Also the relationship of polymorphisms of genes ACE, AT1R, NOS and hANP was described in relation to the development of hypertension which is an important risk factor for macrovascular and microvascular complications of diabetes. In some investigations the relationship of polymorphisms of ACE and AT1R genes and the development of diabetic nephropathy was described where a significant acceleration of the process of atherogenesis occurs. As type 2 diabetes mellitus and atherosclerosis are polygenically determinal diseases, it will be in particular necessary to investigate in future the concurrent influence of several gene polymorphisms and their interactions with the diabetic milieu intérieur on the development of macrovascular and microvascular complications of diabetes.

• MeSH
• angiotensin konvertující enzym genetika   MeSH
• angiotensinogen genetika   MeSH
• arterioskleróza patofyziologie   MeSH
• atriální natriuretický faktor genetika   MeSH
• cévní endotel patofyziologie   MeSH
• diabetes mellitus 2. typu genetika   patofyziologie   MeSH
• diabetické angiopatie genetika   patofyziologie   MeSH
• krevní tlak * genetika   MeSH
• lidé MeSH
• polymorfismus genetický * MeSH
• receptory angiotensinu genetika   MeSH
• renin-angiotensin systém genetika   MeSH
• rizikové faktory MeSH
• synthasa oxidu dusnatého genetika   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• anglický abstrakt MeSH
• časopisecké články MeSH
• přehledy MeSH
• Názvy látek
• angiotensin konvertující enzym MeSH
• angiotensinogen MeSH
• atriální natriuretický faktor MeSH
• receptory angiotensinu MeSH
• synthasa oxidu dusnatého MeSH