%0 Journal Article
%A Veltkamp, Roland
%A Uhlmann, Stefan
%A Marinescu, Marilena
%A Sticht, Carsten
%A Finke, Daniel
%A Gretz, Norbert
%A Gröne, Herrmann-Josef
%A Katus, Hugo A
%A Backs, Johannes
%A Lehmann, Lorenz H
%T Experimental ischaemic stroke induces transient cardiac atrophy and dysfunction.
%J Journal of cachexia, sarcopenia and muscle
%V 10
%N 1
%@ 2190-5991
%C Hoboken, NJ
%I Wiley
%M DKFZ-2018-01844
%P 54-62
%D 2019
%X Stroke can lead to cardiac dysfunction in patients, but the mechanisms underlying the interaction between the injured brain and the heart are poorly understood. The objective of the study is to investigate the effects of experimental murine stroke on cardiac function and molecular signalling in the heart.Mice were subjected to filament-induced left middle cerebral artery occlusion for 30 or 60 min or sham surgery and underwent repetitive micro-echocardiography. Left ventricular contractility was reduced early (24-72 h) but not late (2 months) after brain ischaemia. Cardiac dysfunction was accompanied by a release of high-sensitive cardiac troponin (hsTNT (ng/ml): d1: 7.0 ± 1.0 vs. 25.0 ± 3.2*; d3: 7.3 ± 1.1 vs. 52.2 ± 16.7*; d14: 5.7 ± 0.8 vs. 5.2 ± 0.3; sham vs. 60 min. MCAO; mean ± SEM; *p < 0.05); reduced heart weight (heart weight/tibia length ratio: d1: 6.9 ± 0.2 vs. 6.4 ± 0.1*; d3: 6.7 ± 0.2 vs. 5.8 ± 0.1*; d14: 6.7 ± 0.2 vs. 6.4 ± 03; sham vs. 60 min. MCAO; mean ± SEM; *p < 0.05); resulting from cardiomyocyte atrophy (cardiomyocyte size: d1: 12.8
%F PUB:(DE-HGF)16
%9 Journal Article
%$ pmid:30378296
%R 10.1002/jcsm.12335
%U https://inrepo02.dkfz.de/record/141325