Response of various conduit arteries in tachycardia- and volume overload-induced heart failure.

Although hemodynamics changes occur in heart failure (HF) and generally influence vascular function, it is not clear whether various HF models will affect the conduit vessels differentially or whether local hemodynamic forces or systemic factors are more important determinants of vascular response i...

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Autores principales:	Xiao Lu, Zhen-Du Zhang, Xiaomei Guo, Jenny Susana Choy, Junrong Yang, Mark Svendsen, Ghassan Kassab
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2014
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/924f2e8beaa94518a7375ed5bbabc802
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spelling	oai:doaj.org-article:924f2e8beaa94518a7375ed5bbabc8022021-11-25T06:04:31ZResponse of various conduit arteries in tachycardia- and volume overload-induced heart failure.1932-620310.1371/journal.pone.0101645https://doaj.org/article/924f2e8beaa94518a7375ed5bbabc8022014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/25127035/?tool=EBIhttps://doaj.org/toc/1932-6203Although hemodynamics changes occur in heart failure (HF) and generally influence vascular function, it is not clear whether various HF models will affect the conduit vessels differentially or whether local hemodynamic forces or systemic factors are more important determinants of vascular response in HF. Here, we studied the hemodynamic changes in tachycardia or volume-overload HF swine model (created by either high rate pacing or distal abdominal aortic-vena cava fistula, respectively) on carotid, femoral, and renal arteries function and molecular expression. The ejection fraction was reduced by 50% or 30% in tachycardia or volume-overload model in four weeks, respectively. The LV end diastolic volume was increased from 65 ± 22 to 115 ± 78 ml in tachycardia and 67 ± 19 to 148 ± 68 ml in volume-overload model. Flow reversal was observed in diastolic phase in carotid artery of both models and femoral artery in volume-overload model. The endothelial function was also significantly impaired in carotid and renal arteries of tachycardia and volume-overload animals. The endothelial dysfunction was observed in femoral artery of volume-overload animals but not tachycardia animals. The adrenergic receptor-dependent contractility decreased in carotid and femoral arteries of tachycardia animals. The protein expressions of NADPH oxidase subunits increased in the three arteries and both animal models while expression of MnSOD decreased in carotid artery of tachycardia and volume-overload model. In conclusion, different HF models lead to variable arterial hemodynamic changes but similar vascular and molecular expression changes that reflect the role of both local hemodynamics as well as systemic changes in HF.Xiao LuZhen-Du ZhangXiaomei GuoJenny Susana ChoyJunrong YangMark SvendsenGhassan KassabPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 8, p e101645 (2014)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Xiao Lu Zhen-Du Zhang Xiaomei Guo Jenny Susana Choy Junrong Yang Mark Svendsen Ghassan Kassab Response of various conduit arteries in tachycardia- and volume overload-induced heart failure.
description	Although hemodynamics changes occur in heart failure (HF) and generally influence vascular function, it is not clear whether various HF models will affect the conduit vessels differentially or whether local hemodynamic forces or systemic factors are more important determinants of vascular response in HF. Here, we studied the hemodynamic changes in tachycardia or volume-overload HF swine model (created by either high rate pacing or distal abdominal aortic-vena cava fistula, respectively) on carotid, femoral, and renal arteries function and molecular expression. The ejection fraction was reduced by 50% or 30% in tachycardia or volume-overload model in four weeks, respectively. The LV end diastolic volume was increased from 65 ± 22 to 115 ± 78 ml in tachycardia and 67 ± 19 to 148 ± 68 ml in volume-overload model. Flow reversal was observed in diastolic phase in carotid artery of both models and femoral artery in volume-overload model. The endothelial function was also significantly impaired in carotid and renal arteries of tachycardia and volume-overload animals. The endothelial dysfunction was observed in femoral artery of volume-overload animals but not tachycardia animals. The adrenergic receptor-dependent contractility decreased in carotid and femoral arteries of tachycardia animals. The protein expressions of NADPH oxidase subunits increased in the three arteries and both animal models while expression of MnSOD decreased in carotid artery of tachycardia and volume-overload model. In conclusion, different HF models lead to variable arterial hemodynamic changes but similar vascular and molecular expression changes that reflect the role of both local hemodynamics as well as systemic changes in HF.
format	article
author	Xiao Lu Zhen-Du Zhang Xiaomei Guo Jenny Susana Choy Junrong Yang Mark Svendsen Ghassan Kassab
author_facet	Xiao Lu Zhen-Du Zhang Xiaomei Guo Jenny Susana Choy Junrong Yang Mark Svendsen Ghassan Kassab
author_sort	Xiao Lu
title	Response of various conduit arteries in tachycardia- and volume overload-induced heart failure.
title_short	Response of various conduit arteries in tachycardia- and volume overload-induced heart failure.
title_full	Response of various conduit arteries in tachycardia- and volume overload-induced heart failure.
title_fullStr	Response of various conduit arteries in tachycardia- and volume overload-induced heart failure.
title_full_unstemmed	Response of various conduit arteries in tachycardia- and volume overload-induced heart failure.
title_sort	response of various conduit arteries in tachycardia- and volume overload-induced heart failure.
publisher	Public Library of Science (PLoS)
publishDate	2014
url	https://doaj.org/article/924f2e8beaa94518a7375ed5bbabc802
work_keys_str_mv	AT xiaolu responseofvariousconduitarteriesintachycardiaandvolumeoverloadinducedheartfailure AT zhenduzhang responseofvariousconduitarteriesintachycardiaandvolumeoverloadinducedheartfailure AT xiaomeiguo responseofvariousconduitarteriesintachycardiaandvolumeoverloadinducedheartfailure AT jennysusanachoy responseofvariousconduitarteriesintachycardiaandvolumeoverloadinducedheartfailure AT junrongyang responseofvariousconduitarteriesintachycardiaandvolumeoverloadinducedheartfailure AT marksvendsen responseofvariousconduitarteriesintachycardiaandvolumeoverloadinducedheartfailure AT ghassankassab responseofvariousconduitarteriesintachycardiaandvolumeoverloadinducedheartfailure
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Response of various conduit arteries in tachycardia- and volume overload-induced heart failure.

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