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甲状腺激素受体α1和β1在大鼠心肌梗死后下调:对缺血再灌注反应的影响。

Thyroid hormone receptors alpha1 and beta1 are downregulated in the post-infarcted rat heart: consequences on the response to ischaemia-reperfusion.

作者信息

Pantos C, Mourouzis I, Saranteas T, Paizis I, Xinaris C, Malliopoulou V, Cokkinos D V

机构信息

Department of Pharmacology, University of Athens, 75 Mikras Asias Ave., 11527 Goudi, Athens, Greece.

出版信息

Basic Res Cardiol. 2005 Sep;100(5):422-32. doi: 10.1007/s00395-005-0545-4.

Abstract

There is accumulating evidence that thyroid hormone metabolism is altered after myocardial infarction (AMI) but its physiological relevance remains largely unknown. The present study investigated the possible role of thyroid hormone signaling in the response of the post-infarcted heart to ischaemia-reperfusion. Wistar rats were subjected to left coronary artery ligation (AMI), or sham operation (SHAM). After 8 weeks, hearts from AMI and SHAM rats were perfused in Langendorff mode and subjected to 20 min of zero-flow global ischaemia (I) and 45 min of reperfusion (R); AMI(I/R), n = 7 and SHAM(I/R), n = 7. Basal left ventricular pressure (LVDP), +dp/dt, and -dp/dt were significantly reduced. Left ventricular weight of the viable myocardium was increased by 14% in the AMI as compared to SHAM hearts, P < 0.05. T(3) and T(4) plasma levels in nM were 1.83 (0.08) and 53.3 (2.9) for SHAM and 1.76 (0.06) and 59.4 (5.2) for AMI rats, respectively, P > 0.05. TRalpha1 and TRbeta1 expression levels were 1.3- and 1.8-fold less in AMI than in SHAM hearts, P < 0.05. Furthermore, SERCA and NHE1 expression levels were 2.1- and 1.8-fold less in AMI than in SHAM, P < 0.05. PKCepsilon was 1.35-fold more in AMI compared to SHAM, P < 0.05. Myocardial glycogen content (in micromol/g) was 7.8 (1.2) in AMI as compared to 4.4 (0.5) for SHAM hearts, P < 0.05. After I/R, left ventricular end-diastolic pressure at 45 min of R (LVEDP45 in mmHg) was 20.3 (3.2) for AMI(I/R) vs 50.6 (4.8) mmHg for SHAM(I/R), P < 0.05. LDH release per gram of tissue was 251 (103) for AMI(I/R) and 762 (74) for SHAM(I/R), P < 0.05. In conclusion, TRalpha1 and TRbeta1 are downregulated after myocardial infarction and this was associated with altered expression of thyroid hormone responsive genes and increased tolerance of the post-infarcted heart to ischaemia-reperfusion injury.

摘要

越来越多的证据表明,心肌梗死(AMI)后甲状腺激素代谢会发生改变,但其生理相关性在很大程度上仍不清楚。本研究调查了甲状腺激素信号在梗死心脏对缺血再灌注反应中的可能作用。将Wistar大鼠进行左冠状动脉结扎(AMI)或假手术(SHAM)。8周后,将AMI和SHAM大鼠的心脏以Langendorff模式灌注,并进行20分钟的零流量全心缺血(I)和45分钟的再灌注(R);AMI(I/R),n = 7,SHAM(I/R),n = 7。基础左心室压力(LVDP)、+dp/dt和 -dp/dt显著降低。与SHAM心脏相比,AMI中存活心肌的左心室重量增加了14%,P < 0.05。SHAM大鼠的血浆T(3)和T(4)水平(以nM计)分别为1.83(0.08)和53.3(2.9),AMI大鼠分别为1.76(0.06)和59.4(5.2),P > 0.05。AMI中TRalpha1和TRbeta1的表达水平分别比SHAM心脏低1.3倍和1.8倍,P < 0.05。此外,AMI中SERCA和NHE1的表达水平分别比SHAM低2.1倍和1.8倍,P < 0.05。与SHAM相比,AMI中PKCepsilon增加了1.35倍,P < 0.05。AMI中心肌糖原含量(以微摩尔/克计)为7.8(1.2),而SHAM心脏为4.4(0.5),P < 0.05。I/R后,R 45分钟时的左心室舒张末期压力(LVEDP45,以mmHg计),AMI(I/R)为20.3(3.2),SHAM(I/R)为50.6(4.8)mmHg,P < 0.05。每克组织的LDH释放量,AMI(I/R)为251(103),SHAM(I/R)为762(74),P < 0.05。总之,心肌梗死后TRalpha1和TRbeta1下调,这与甲状腺激素反应基因的表达改变以及梗死心脏对缺血再灌注损伤的耐受性增加有关。

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