FRINK Linked Data Fragments server

Matches in SemOpenAlex for { <https://semopenalex.org/work/W2032357416> ?p ?o ?g. }

• W2032357416 endingPage "746" @default.
• W2032357416 startingPage "742" @default.
• W2032357416 abstract "ObjectiveRecent studies have shown that mechanically unloading a failing heart may induce reverse remodeling and functional improvement. However, these benefits may be balanced by an unloading-related remodeling including myocardial atrophy that might lead to decrease in function. Using a model of heterotopic heart transplantation, we aimed to characterize the myocardial changes induced by long-term unloading.Material and MethodsMacroscopic as well as cellular and functional changes were followed in normal hearts unloaded for a 3-month period. Microscopic parameters were evaluated with stereologic methodology. Myocardial contractile function was quantified with a Langendorff isolated, perfused heart technique.ResultsAtrophy was macroscopically obvious and accompanied by a 67% reduction of the myocyte volume and a 43% reduction of the interstitial tissue volume, thus accounting for a shift of the myocyte/connective tissue ratio in favor of noncontractile tissue. The absolute number of cardiomyocyte nuclei decreased from 64.7 ± 5.1 × 107 in controls to 22.6 ± 3.7 × 107 (30 days) and 21.6 ± 3.1 × 107 (90 days) after unloading (P < .05). The numeric nucleic density in the unloaded myocardium, as well as the mean cardiomyocyte volume per cardiomyocyte nucleus, remained constant throughout the 90 days of observation. Functional data indicated an increase in ventricular stiffness, although contractile function was preserved, as confirmed by unaltered maximal developed pressure and increased contractility (maximum rate of left ventricular pressure development) and relaxation (minimum rate of left ventricular pressure development).ConclusionAtrophic remodeling involves both the myocyte and interstitial tissue compartment. These data suggest that although there is decreased myocardial volume and increased stiffness, contractile capacity is preserved in the long-term unloaded heart. Recent studies have shown that mechanically unloading a failing heart may induce reverse remodeling and functional improvement. However, these benefits may be balanced by an unloading-related remodeling including myocardial atrophy that might lead to decrease in function. Using a model of heterotopic heart transplantation, we aimed to characterize the myocardial changes induced by long-term unloading. Macroscopic as well as cellular and functional changes were followed in normal hearts unloaded for a 3-month period. Microscopic parameters were evaluated with stereologic methodology. Myocardial contractile function was quantified with a Langendorff isolated, perfused heart technique. Atrophy was macroscopically obvious and accompanied by a 67% reduction of the myocyte volume and a 43% reduction of the interstitial tissue volume, thus accounting for a shift of the myocyte/connective tissue ratio in favor of noncontractile tissue. The absolute number of cardiomyocyte nuclei decreased from 64.7 ± 5.1 × 107 in controls to 22.6 ± 3.7 × 107 (30 days) and 21.6 ± 3.1 × 107 (90 days) after unloading (P < .05). The numeric nucleic density in the unloaded myocardium, as well as the mean cardiomyocyte volume per cardiomyocyte nucleus, remained constant throughout the 90 days of observation. Functional data indicated an increase in ventricular stiffness, although contractile function was preserved, as confirmed by unaltered maximal developed pressure and increased contractility (maximum rate of left ventricular pressure development) and relaxation (minimum rate of left ventricular pressure development). Atrophic remodeling involves both the myocyte and interstitial tissue compartment. These data suggest that although there is decreased myocardial volume and increased stiffness, contractile capacity is preserved in the long-term unloaded heart." @default.
• W2032357416 created "2016-06-24" @default.
• W2032357416 creator A5003986527 @default.
• W2032357416 creator A5014714790 @default.
• W2032357416 creator A5026311765 @default.
• W2032357416 creator A5033908729 @default.
• W2032357416 creator A5047459039 @default.
• W2032357416 creator A5050161918 @default.
• W2032357416 creator A5090160176 @default.
• W2032357416 date "2009-03-01" @default.
• W2032357416 modified "2023-10-03" @default.
• W2032357416 title "Contractile function is preserved in unloaded hearts despite atrophic remodeling" @default.
• W2032357416 cites W1970031998 @default.
• W2032357416 cites W1972932733 @default.
• W2032357416 cites W1972962885 @default.
• W2032357416 cites W1979818151 @default.
• W2032357416 cites W1996753402 @default.
• W2032357416 cites W2008434058 @default.
• W2032357416 cites W2009419574 @default.
• W2032357416 cites W2014167331 @default.
• W2032357416 cites W2023997583 @default.
• W2032357416 cites W2027393528 @default.
• W2032357416 cites W2028163205 @default.
• W2032357416 cites W2038524881 @default.
• W2032357416 cites W2039087506 @default.
• W2032357416 cites W2048184684 @default.
• W2032357416 cites W2054839386 @default.
• W2032357416 cites W2056804173 @default.
• W2032357416 cites W2072904295 @default.
• W2032357416 cites W2073873067 @default.
• W2032357416 cites W2074579539 @default.
• W2032357416 cites W2081236923 @default.
• W2032357416 cites W2103564980 @default.
• W2032357416 cites W2115607473 @default.
• W2032357416 cites W2138080145 @default.
• W2032357416 cites W2146942902 @default.
• W2032357416 cites W2157460773 @default.
• W2032357416 cites W2161309614 @default.
• W2032357416 cites W2167840127 @default.
• W2032357416 cites W2172010440 @default.
• W2032357416 cites W2278138507 @default.
• W2032357416 doi "https://doi.org/10.1016/j.jtcvs.2008.09.020" @default.
• W2032357416 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/19258100" @default.
• W2032357416 hasPublicationYear "2009" @default.
• W2032357416 type Work @default.
• W2032357416 sameAs 2032357416 @default.
• W2032357416 citedByCount "27" @default.
• W2032357416 countsByYear W20323574162012 @default.
• W2032357416 countsByYear W20323574162013 @default.
• W2032357416 countsByYear W20323574162014 @default.
• W2032357416 countsByYear W20323574162015 @default.
• W2032357416 countsByYear W20323574162016 @default.
• W2032357416 countsByYear W20323574162017 @default.
• W2032357416 countsByYear W20323574162018 @default.
• W2032357416 countsByYear W20323574162019 @default.
• W2032357416 countsByYear W20323574162022 @default.
• W2032357416 countsByYear W20323574162023 @default.
• W2032357416 crossrefType "journal-article" @default.
• W2032357416 hasAuthorship W2032357416A5003986527 @default.
• W2032357416 hasAuthorship W2032357416A5014714790 @default.
• W2032357416 hasAuthorship W2032357416A5026311765 @default.
• W2032357416 hasAuthorship W2032357416A5033908729 @default.
• W2032357416 hasAuthorship W2032357416A5047459039 @default.
• W2032357416 hasAuthorship W2032357416A5050161918 @default.
• W2032357416 hasAuthorship W2032357416A5090160176 @default.
• W2032357416 hasBestOaLocation W20323574161 @default.
• W2032357416 hasConcept C126322002 @default.
• W2032357416 hasConcept C142724271 @default.
• W2032357416 hasConcept C164705383 @default.
• W2032357416 hasConcept C207200792 @default.
• W2032357416 hasConcept C2778198053 @default.
• W2032357416 hasConcept C2778849806 @default.
• W2032357416 hasConcept C2779537366 @default.
• W2032357416 hasConcept C2781172350 @default.
• W2032357416 hasConcept C39133596 @default.
• W2032357416 hasConcept C518705261 @default.
• W2032357416 hasConcept C71924100 @default.
• W2032357416 hasConceptScore W2032357416C126322002 @default.
• W2032357416 hasConceptScore W2032357416C142724271 @default.
• W2032357416 hasConceptScore W2032357416C164705383 @default.
• W2032357416 hasConceptScore W2032357416C207200792 @default.
• W2032357416 hasConceptScore W2032357416C2778198053 @default.
• W2032357416 hasConceptScore W2032357416C2778849806 @default.
• W2032357416 hasConceptScore W2032357416C2779537366 @default.
• W2032357416 hasConceptScore W2032357416C2781172350 @default.
• W2032357416 hasConceptScore W2032357416C39133596 @default.
• W2032357416 hasConceptScore W2032357416C518705261 @default.
• W2032357416 hasConceptScore W2032357416C71924100 @default.
• W2032357416 hasIssue "3" @default.
• W2032357416 hasLocation W20323574161 @default.
• W2032357416 hasLocation W20323574162 @default.
• W2032357416 hasOpenAccess W2032357416 @default.
• W2032357416 hasPrimaryLocation W20323574161 @default.
• W2032357416 hasRelatedWork W2009308266 @default.
• W2032357416 hasRelatedWork W2068259322 @default.
• W2032357416 hasRelatedWork W2088188662 @default.
• W2032357416 hasRelatedWork W2356526470 @default.
• W2032357416 hasRelatedWork W2407717929 @default.

• next