Abstract:
:The heart is subjected to chronic mechanical unloading during prolonged spaceflight and microgravity. The heart in patients with end-stage heart failure is also unloaded in prolonged duration after left ventricular assist devices (LVAD) are implanted. Heterotopic heart transplantation in rats is an established model of chronic cardiac unloading, and has been used to investigate the effects of chronic cardiac unloading on the heart. Observations that have been found using this experimental model are as follow. Chronic cardiac unloading induces time-dependent depressions of Ca2+ handling and myocyte contractility, which are associated with the shift of myosin heavy chain (MHC) isozymes and altered expressions of Ca2+ cycling-related proteins. Treatment with the physiological treatment dose of thyroid hormone restores the expression levels of Ca2+ cycling-related proteins, Ca2+ handling, and contractile function of cardiac myocytes in chronically unloaded hearts. Although future studies are required to determine precise mechanisms of the beneficial effects of thyroid hormone on chronically unloaded hearts, these observations may have clinical implications in the future for chronic cardiac unloading in the space industry as well as in the treatment of patients with end-stage heart failure supported by LVAD.
journal_name
Vascul Pharmacoljournal_title
Vascular pharmacologyauthors
Ito K,Kagaya Y,Shimokawa Hdoi
10.1016/j.vph.2009.10.004subject
Has Abstractpub_date
2010-03-01 00:00:00pages
138-41issue
3-4eissn
1537-1891issn
1879-3649pii
S1537-1891(09)00124-4journal_volume
52pub_type
杂志文章,评审abstract::We previously showed that endothelin A (ETA) receptor antagonist BQ-123 partially inhibited cyclopiazonic acid (CPA)-enhanced endothelin-1 (ET-1)-induced contractions suggesting enhancement of ETA receptor internalization in caveolar structures by sarco/endoplasmic reticulum Ca+2 ATPase (SERCA) blockade. Since seroton...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2014.03.008
更新日期:2014-05-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2014.05.011
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abstract:RATIONALE:We examined the role of Jak2 kinase phosphorylation in the development of pressure overload hypertrophy in mice subjected to transverse aortic constriction (TAC) and treated with tyrphostin AG490, a pharmacological inhibitor of Jak2. METHODS:Control mice (sham), subjected to TAC for 15 days (TAC) or to TAC a...
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doi:10.1016/j.vph.2006.05.006
更新日期:2006-12-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.07.003
更新日期:2010-09-01 00:00:00
abstract::Evidence from both clinical and experimental studies indicates that Di-peptidyl peptidase-IV (DPP-4) inhibition may mediate favorable effects on the cardiovascular system. The objective of this study was to examine the acute effects of DPP-4 inhibition on vascular responses and to study the underlying mechanisms of al...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2011.03.001
更新日期:2011-07-01 00:00:00
abstract::The endothelium synthesizes and releases nitric oxide (NO) to maintain homeostatic function. Under basal conditions, endothelium-derived NO maintains a nonthrombogenic surface, prohibits leukocyte attachment, and promotes vascular relaxation. In the setting of clinical syndromes associated with the development of athe...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/s1537-1891(02)00250-1
更新日期:2002-05-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2011.07.004
更新日期:2011-10-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2014.01.003
更新日期:2014-02-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.02.005
更新日期:2016-07-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/s1537-1891(03)00051-x
更新日期:2003-10-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2015.02.017
更新日期:2015-04-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2005.11.006
更新日期:2006-04-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.10.002
更新日期:2007-03-01 00:00:00
abstract:OBJECTIVES:This study examined the role of Na+/K+-ATPase in the vasodilator actions of nitric oxide (NO), S-nitrosothiols and the endothelium-dependent agonist, acetylcholine. METHODS:The vasodilator responses elicited by intravenous injections of (i) the NO-donors, sodium nitroprusside and MAHMA NONOate, (ii) the S-n...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.06.008
更新日期:2006-12-01 00:00:00
abstract::Increased TNFα-mediated JNK signaling in the perivascular adipose tissue (PVAT) may contribute to the pathogenesis of vascular complications in T1DM by reducing adiponectin (Ad) synthesis and therefore impairing Ad-mediated activity in the contiguous blood vessel system. We evaluated whether in vivo treatment with the...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2016.08.007
更新日期:2016-12-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2017.09.007
更新日期:2017-12-01 00:00:00
abstract:AIM:Selenium, a trace element involved in important enzymatic activities inside the body, has protective effects against cardiovascular diseases including atherosclerosis. The safe dose of selenium in the organism is very narrow, limiting the supplementation of selenium in diet. The aim of this study is to explore whet...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2019.01.005
更新日期:2019-04-01 00:00:00
abstract::Phosphorylation of proteins on tyrosine acts as a reversible and specific trigger mechanism, forming or disrupting regulatory connections between proteins. Tyrosine kinases and phosphatases participate in multiple cellular processes, and considerable evidence now supports a role for tyrosine phosphorylation in vascula...
journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/s1537-1891(03)00009-0
更新日期:2002-11-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.08.001
更新日期:2010-11-01 00:00:00
abstract::Endothelin (ET-1) is chronically elevated in diabetes. However, role of ET-1 in increased oxidative stress in type 2 diabetes is less clear. This study tested the hypotheses that: 1) oxidative stress markers are increased and total antioxidant capacity is decreased in diabetes, and 2) activation of ET(A) receptors med...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2007.05.006
更新日期:2007-08-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2018.08.011
更新日期:2019-01-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2017.11.002
更新日期:2018-02-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 临床试验,杂志文章,随机对照试验
doi:10.1016/s1537-1891(02)00300-2
更新日期:2002-08-01 00:00:00
abstract::The antiatherosclerotic effects of the dihydropyridine-type calcium channel blocker, benidipine hydrochloride (benidipine), and 3-hydroxy-3-methylglutaryl coenzyme A reductase inhibitor, pravastatin sodium (pravastatin), were compared in hypercholesterolemic rabbits. Male, New Zealand white rabbits were fed a 0.5% cho...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2006.11.004
更新日期:2007-04-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2010.09.001
更新日期:2010-11-01 00:00:00
abstract::We have previously reported that prolonged exposure of porcine coronary arteries to adenosine agonists upregulates protein kinase C (PKC) through the activation of adenosine A1 receptor-coupled to pertussis toxin sensitive G-protein(s) [Am. J. Physiol. 264 (1993) H1465; Am. J. Physiol. 269 (1995) H1619]. The mechanism...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/s1537-1891(02)00307-5
更新日期:2002-07-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2015.10.010
更新日期:2016-06-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章,评审
doi:10.1016/j.vph.2014.10.006
更新日期:2014-12-01 00:00:00
abstract:BACKGROUND:Altered endothelial cell (EC)-derived mediator levels, including increased endothelin-1 (ET-1), are hallmarks of human pulmonary arterial hypertension (PAH). Gene mutations for receptors for bone morphogenic proteins (BMP), or transforming growth factor-beta (TGF-beta) cause heritable PAH. The effects of BMP...
journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2008.09.001
更新日期:2009-01-01 00:00:00
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journal_title:Vascular pharmacology
pub_type: 杂志文章
doi:10.1016/j.vph.2019.106601
更新日期:2020-01-01 00:00:00