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Transverse aortic constriction

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https://www.readbyqxmd.com/read/28528655/pulmonary-flow-as-an-improved-method-for-determining-cardiac-output-in-mice-after-myocardial-infarction
#1
Mathew J Platt, Jason S Huber, Keith R Brunt, Jeremy A Simpson
BACKGROUND: Echocardiography is a valuable noninvasive technique to estimate cardiac output (CO) from the left ventricle (LV) not only in clinical practice but also in small-animal experiments. CO is used to grade cardiac function and is especially important when investigating cardiac injury (e.g., myocardial infarction [MI]). Critically, MI deforms the LV, invalidating the assumptions fundamental to calculating of cardiac volumes directly from the LV. Thus, the purpose of this study was to determine if Doppler-derived blood flow through the pulmonary trunk (pulmonary flow [PF]) was an improved method over conventional LV-dependent echocardiography to accurately determine CO after MI...
June 2017: Journal of the American Society of Echocardiography
https://www.readbyqxmd.com/read/28526353/stretch-activated-two-pore-domain-k2p-potassium-channels-in-the-heart-focus-on-atrial-fibrillation-and-heart-failure
#2
REVIEW
Constanze Schmidt, Felix Wiedmann, Stefan M Kallenberger, Antonius Ratte, Jan S Schulte, Beatrix Scholz, Frank Ulrich Müller, Niels Voigt, Maria-Patapia Zafeiriou, Joachim R Ehrlich, Ursula Tochtermann, Gábor Veres, Arjang Ruhparwar, Matthias Karck, Hugo A Katus, Dierk Thomas
Two-pore-domain potassium (K2P) channels modulate cellular excitability. The significance of stretch-activated cardiac K2P channels (K2P2.1, TREK-1, KCNK2; K2P4.1, TRAAK, KCNK4; K2P10.1, TREK-2, KCNK10) in heart disease has not been elucidated in detail. The aim of this work was to assess expression and remodeling of mechanosensitive K2P channels in atrial fibrillation (AF) and heart failure (HF) patients in comparison to murine models. Cardiac K2P channel levels were quantified in atrial (A) and ventricular (V) tissue obtained from patients undergoing open heart surgery...
May 16, 2017: Progress in Biophysics and Molecular Biology
https://www.readbyqxmd.com/read/28503736/hydrogen-sulfide-pretreatment-improves-mitochondrial-function-in-myocardial-hypertrophy-via-a-sirt3-dependent-manner
#3
Guoliang Meng, Jieqiong Liu, Shangmin Liu, Qiuyi Song, Lulu Liu, Liping Xie, Yi Han, Yong Ji
BACKGROUND AND PURPOSE Hydrogen sulfide (H2 S) is a gaseous signal molecule with anti-oxidative ability. Sirtuin 3 (SIRT3) is closely associated with mitochondrial function and oxidative stress. The study was to investigate whether and how H2 S improved myocardial hypertrophy via a SIRT3-dependent manner. EXPERIMENTAL APPROACH Neonatal rat cardiomyocytes were pre-treated with NaHS (50 μM) for 4 h followed by angiotensin II (Ang II, 100 nM) for 24 h. SIRT3 was silenced with siRNA technology. SIRT 3 promoter activity and expression, cell surface, hypertrophic gene mRNA expression, mitochondrial oxygen consumption rate and membrane potential were measured...
May 15, 2017: British Journal of Pharmacology
https://www.readbyqxmd.com/read/28494450/stachydrine-protects-against-pressure-overload-induced-cardiac-hypertrophy-by-suppressing-autophagy
#4
Tong-Tong Cao, Hui-Hua Chen, Zhiwei Dong, Yan-Wu Xu, Pei Zhao, Wei Guo, Hong-Chang Wei, Chen Zhang, Rong Lu
BACKGROUND: Autophagy is required for the maintenance of cardiomyocyte homeostasis. However, excessive autophagy plays a maladaptive role in pressure overload-induced heart failure. To identify mechanisms by which Stachydrine inhibits pressure overload-induced cardiac hypertrophy, we determined inhibitory activities against activation of NADPH oxidase, reactive oxygen species(ROS) production and excessive activation of autophagy. METHODS: Stachydrine was administered intragastrically to Wistar rats after Transverse aortic constriction(TAC) and H9c2 cells were treated with Stachydrine after Angiotension II stimulation...
May 11, 2017: Cellular Physiology and Biochemistry
https://www.readbyqxmd.com/read/28491305/effects-of-carvedilol-on-structural-and-functional-outcomes-and-plasma-biomarkers-in-the-mouse-transverse-aortic-constriction-heart-failure-model
#5
Caryn Hampton, Raymond Rosa, Daphne Szeto, Gail Forrest, Barry Campbell, Richard Kennan, Shubing Wang, Chin-Hu Huang, Loise Gichuru, Xiaoli Ping, Xiaolan Shen, Kersten Small, Jeffrey Madwed, Joseph J Lynch
INTRODUCTION: Despite the widespread use of the mouse transverse aortic constriction heart failure model, there are no reports on the characterization of the standard-of-care agent carvedilol in this model. METHODS: Left ventricular pressure overload was produced in mice by transverse aortic constriction between the innominate and left common carotid arteries. Carvedilol was administered at multiple dose levels (3, 10 and 30 mg/kg/day per os; yielding end-study mean plasma concentrations of 0...
2017: SAGE Open Medicine
https://www.readbyqxmd.com/read/28487390/activation-of-the-amino-acid-response-pathway-blunts-the-effects-of-cardiac-stress
#6
Pu Qin, Pelin Arabacilar, Roberta E Bernard, Weike Bao, Alan R Olzinski, Yuanjun Guo, Hind Lal, Stephen H Eisennagel, Michael C Platchek, Wensheng Xie, Julius Del Rosario, Mohamad Nayal, Quinn Lu, Theresa Roethke, Christine G Schnackenberg, Fe Wright, Michael P Quaile, Wendy S Halsey, Ashley M Hughes, Ganesh M Sathe, George P Livi, Robert B Kirkpatrick, Xiaoyan A Qu, Deepak K Rajpal, Maria Faelth Savitski, Marcus Bantscheff, Gerard Joberty, Giovanna Bergamini, Thomas L Force, Gregory J Gatto, Erding Hu, Robert N Willette
BACKGROUND: The amino acid response (AAR) is an evolutionarily conserved protective mechanism activated by amino acid deficiency through a key kinase, general control nonderepressible 2. In addition to mobilizing amino acids, the AAR broadly affects gene and protein expression in a variety of pathways and elicits antifibrotic, autophagic, and anti-inflammatory activities. However, little is known regarding its role in cardiac stress. Our aim was to investigate the effects of halofuginone, a prolyl-tRNA synthetase inhibitor, on the AAR pathway in cardiac fibroblasts, cardiomyocytes, and in mouse models of cardiac stress and failure...
May 9, 2017: Journal of the American Heart Association
https://www.readbyqxmd.com/read/28464037/pressure-overload-induced-angiotensin-mediated-early-remodeling-in-mouse-heart
#7
Jeremy H Kim, Ya-Ping Jiang, Ira S Cohen, Richard Z Lin, Richard T Mathias
Our previous work on angiotensin II-mediated electrical-remodeling in canine left ventricle, in connection with a long history of other studies, suggested the hypothesis: increases in mechanical load induce autocrine secretion of angiotensin II (A2), which coherently regulates a coterie of membrane ion transporters in a manner that increases contractility. However, the relation between load and A2 secretion was correlative. We subsequently showed a similar or identical system was present in murine heart. To investigate whether the relation between mechanical load and A2-mediated electrical remodeling was causal, we employed transverse aortic constriction in mice to subject the left ventricle to pressure overload for short-term (1 to 2 days) or long-term (1 to 2 weeks) periods...
2017: PloS One
https://www.readbyqxmd.com/read/28455286/ultrasound-biomicroscopy-validation-of-a-murine-model-of-cardiac-hypertrophic-preconditioning-comparison-with-a-hemodynamic-assessment
#8
Jiayuan Huang, Jian Wu, Shijun Wang, Jieyun You, Yong Ye, Zhiwen Ding, Fenghua Yang, Xingxu Wang, Junjie Guo, Leilei Ma, Jie Yuan, Yunli Shen, Xiangdong Yang, Aijun Sun, Hong Jiang, Liping Bu, Peter H Backx, Junbo Ge, Yunzeng Zou
In mice, myocardial hypertrophic preconditioning (HP), which is produced by the removal of short-term transverse aortic constriction (TAC), was recently reported to render the heart resistant to hypertrophic responses induced by subsequent re-constriction (Re-TAC). However, there is no efficient non-invasive method for ensuring that the repeated aortic manipulations were successfully performed. We previously demonstrated that ultrasound biomicroscopy (UBM) is a non-invasive and effective approach for predicting TAC success...
April 28, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28450225/ablation-il-33-gene-exacerbate-myocardial-remodeling-in-mice-with-heart-failure-induced-by-mechanical-stress
#9
Punniyakoti T Veeraveedu, Shoji Sanada, Keiji Okuda, Hai Ying Fu, Takashi Matsuzaki, Ryo Araki, Masaki Yamato, Koubun Yasuda, Yasushi Sakata, Tomohiro Yoshimoto, Tetsuo Minamino
BACKGROUND AND PURPOSE: ST2 is one of the interleukin (IL)-1 receptor family member comprising of membrane-bound (ST2L) and soluble (sST2) isoforms. Clinical trials have revealed that serum sST2 levels predict outcome in patient with myocardial infarction or chronic heart failure (HF). Meanwhile, we and others have reported that ablation of ST2 caused exaggerated cardiac remodeling in both ischemic and non-ischemic HF. Here, we tested whether IL-33, the ligand for ST2, protects myocardium against HF induced by mechanical overload using ligand specific knockout (IL-33(-/-)) mice...
April 24, 2017: Biochemical Pharmacology
https://www.readbyqxmd.com/read/28432058/mk5-haplodefficiency-attenuates-hypertrophy-and-preserves-diastolic-function-during-remodeling-induced-by-chronic-pressure-overload-in-the-mouse-heart
#10
Sherin Nawaito, Dharmendra Dingar, Pramod Sahadevan, Bahira Hussein, Fatiha Sahmi, Yanfen Shi, Marc-Antoine Gillis, Matthias Gaestel, Jean-Claude Tardif, Bruce G Allen
MK5 is a protein serine and threonine kinase that is activated by p38 MAPK and the atypical MAPKs ERK3 and ERK4. The physiological function(s) of MK5 remain unknown. Herein we examine the effect of MK5 haplodeficiency on cardiac function and myocardial remodeling. At 12-weeks of age, MK5 haplodeficient mice (MK5(+/-)) were smaller than age-matched wild-type litter mates (MK5(+/+)), with similar diastolic function but reduced systolic function. Transverse aortic constriction (TAC) was employed to induce a chronic pressure overload in twelve-week-old male MK5(+/-) and MK5(+/+) mice...
April 21, 2017: American Journal of Physiology. Heart and Circulatory Physiology
https://www.readbyqxmd.com/read/28426781/tauroursodeoxycholic-acid-tudca-attenuates-pressure-overload-induced-cardiac-remodeling-by-reducing-endoplasmic-reticulum-stress
#11
Shilpa Rani, Pradeep Kumar Sreenivasaiah, Jin Ock Kim, Mi Young Lee, Wan Seok Kang, Yong Sook Kim, Youngkeun Ahn, Woo Jin Park, Chunghee Cho, Do Han Kim
Pressure overload in the heart induces pathological hypertrophy and is associated with cardiac dysfunction. Apoptosis and fibrosis signaling initiated by the endoplasmic reticulum stress (ERS) is known to contribute to these maladaptive effects. The aim of this study was to investigate whether reduction of ERS by a known chemical chaperone, tauroursodeoxycholic acid (TUDCA) can attenuate pressure overload-induced cardiac remodeling in a mouse model of transverse aortic constriction (TAC). Oral administration of TUDCA at a dose of 300 mg/kg body weight (BW) in the TUDCA-TAC group reduced ERS markers (GRP78, p-PERK, and p-eIf2α), compared to the Vehicle (Veh)-TAC group...
2017: PloS One
https://www.readbyqxmd.com/read/28423592/protective-effect-of-hydrogen-sulphide-against-myocardial-hypertrophy-in-mice
#12
Mingjing Shao, Chuanjun Zhuo, Ronghuan Jiang, Guangdong Chen, Jianmin Shan, Jing Ping, Hongjun Tian, Lina Wang, Chongguang Lin, Lirong Hu
Cardiac hypertrophy is a critical component of phenotype in the failing heart. Recently, increasing evidence has demonstrated that oxidative stress plays an important role in the pathogenesis of myocardial hypertrophy. In the present study, we generated a mouse model of transverse aortic constriction (TAC) to investigate whether hydrogen sulfide (H2S) has protective effects against cardiac hypertrophy. Left ventricular structure was analyzed by two-dimensional echocardiography. Oxidative stress was evaluated by measuring malondialdehyde, superoxide dismutase, glutathione peroxidase and reactive oxygen specie in the myocardium...
April 4, 2017: Oncotarget
https://www.readbyqxmd.com/read/28404627/multiphasic-regulation-of-systemic-and-peripheral-organ-metabolic-responses-to-cardiac-hypertrophy
#13
Chong Wee Liew, Shanshan Xu, Xuerong Wang, Maximilian McCann, Hyerim Whang Kong, Andrew C Carley, Jingbo Pang, Giamila Fantuzzi, J Michael O'Donnell, E Douglas Lewandowski
BACKGROUND: Reduced fat oxidation in hypertrophied hearts coincides with a shift of carnitine palmitoyl transferase I from muscle to increased liver isoforms. Acutely increased carnitine palmitoyl transferase I in normal rodent hearts has been shown to recapitulate the reduced fat oxidation and elevated atrial natriuretic peptide message of cardiac hypertrophy. METHODS AND RESULTS: Because of the potential for reduced fat oxidation to affect cardiac atrial natriuretic peptide, and thus, induce adipose lipolysis, we studied peripheral and systemic metabolism in male C57BL/6 mice model of transverse aortic constriction in which left ventricular hypertrophy occurred by 2 weeks without functional decline until 16 weeks (ejection fraction, -45...
April 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/28404626/adenosine-formed-by-cd73-on-t-cells-inhibits-cardiac-inflammation-and-fibrosis-and-preserves-contractile-function-in-transverse-aortic-constriction-induced-heart-failure
#14
Christine Quast, Christina Alter, Zhaoping Ding, Nadine Borg, Jürgen Schrader
BACKGROUND: Structural damage during heart failure development leads to increased infiltration of leukocytes. Because purinergic signaling on immune cells may impact on the inflammatory response, we evaluated the role of ecto-5'-nucleotidase (CD73) on the development of heart failure after transverse aortic constriction (TAC) using global and T-cell-specific CD73(-)(/-) mice. METHODS AND RESULTS: Leukocytes infiltrating the failing heart were analyzed by a multistep enzymatic procedure over a period of 16 weeks using fluorescence-activated cell sorting...
April 2017: Circulation. Heart Failure
https://www.readbyqxmd.com/read/28395201/syndecan-4-deficiency-accelerates-the-transition-from-compensated-hypertrophy-to-heart-failure-following-pressure-overload
#15
Guannan Li, Jun Xie, Jianzhou Chen, Ran Li, Han Wu, Xinlin Zhang, Qinhua Chen, Rong Gu, Biao Xu
Increasing evidence suggests that a mismatch between angiogenesis and myocardial growth contributes to the transition from adaptive cardiac hypertrophy to heart failure following pressure overload. Syndecan-4 is a transmembrane proteoglycan that binds to growth factors and extracellular matrix proteins and is critical in focal adhesion formation. However, its effects on coronary angiogenesis during pressure overload-induced heart failure have not been studied. Here, we hypothesize that syndecan-4 modulates cardiac remodeling in response to pressure overload through its ability to regulate adaptive angiogenesis...
May 2017: Cardiovascular Pathology: the Official Journal of the Society for Cardiovascular Pathology
https://www.readbyqxmd.com/read/28374413/beneficial-effects-of-leptin-treatment-in-a-setting-of-cardiac-dysfunction-induced-by-transverse-aortic-constriction-in-mouse
#16
Nieves Gómez-Hurtado, Alejandro Domínguez-Rodríguez, Philippe Mateo, Maria Fernandez-Velasco, Almudena Val-Blasco, Rafael Aizpún, Jessica Sabourin, Ana Maria Gómez, Jean-Pierre Benitah, Carmen Delgado
KEY POINTS: Leptin, is a 16 kDa pleiotropic peptide, primary secreted by adipocytes, but also produced by other tissues including the heart. Controversy exists regarding the adverse and beneficial effects of Leptin on the heart We analysed the effect of a non-hypertensive dose of leptin on cardiac function, [Ca(2+) ]i handling and cellular electrophysiology, which participate in the genesis of pump failure and related arrhythmias both in control mice and in mice subjected to chronic pressure-overload by transverse aorta constriction We find that Leptin activates mechanisms that contribute to cardiac dysfunction in physiological conditions...
April 4, 2017: Journal of Physiology
https://www.readbyqxmd.com/read/28371893/tissue-transglutaminase-induction-in-the-pressure-overloaded-myocardium-regulates-matrix-remodeling
#17
Arti V Shinde, Marcin Dobaczewski, Judith J de Haan, Amit Saxena, Kang-Kon Lee, Ying Xia, Wei Chen, Ya Su, Waqas Hanif, Inderpreet Kaur Madahar, Victor M Paulino, Gerry Melino, Nikolaos G Frangogiannis
Aims: : Tissue transglutaminase (tTG) is induced in injured and remodeling tissues, and modulates cellular phenotype, while contributing to matrix cross-linking. Our study tested the hypothesis that tTG may be expressed in the pressure-overloaded myocardium, and may regulate cardiac function, myocardial fibrosis and chamber remodeling. Methods and results: In order to test the hypothesis, wildtype and tTG null mice were subjected to pressure overload induced through transverse aortic constriction...
March 28, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28371805/restitution-slope-is-principally-determined-by-steady-state-action-potential-duration
#18
Michael J Shattock, Kyung Chan Park, Hsiang-Yu Yang, Angela W C Lee, Steven Niederer, Kenneth T MacLeod, James Winter
Aims: The steepness of the action potential duration (APD) restitution curve and local tissue refractoriness are both thought to play important roles in arrhythmogenesis. Despite this, there has been little recognition of the apparent association between steady-state APD and the slope of the restitution curve. The objective of this study was to test the hypothesis that restitution slope is determined by APD and to examine the relationship between restitution slope, refractoriness and susceptibility to VF...
June 1, 2017: Cardiovascular Research
https://www.readbyqxmd.com/read/28367092/pkd-knockdown-inhibits-pressure-overload-induced-cardiac-hypertrophy-by-promoting-autophagy-via-akt-mtor-pathway
#19
Di Zhao, Wei Wang, Hao Wang, Honghai Peng, Xiangjuan Liu, Weixing Guo, Guohai Su, Zhuo Zhao
Growing evidence shows that protein kinase D (PKD) plays an important role in the development of pressure overload-induced cardiac hypertrophy. However, the mechanisms involved are not clear. This study tested our hypothesis that PKD might mediate cardiac hypertrophy by negatively regulating autophagy using the technique of PKD knockdown by siRNA. Cardiac hypertrophy was induced in 8-week old male C57BL/6 mice by transverse aortic constriction (TAC). TAC mice were then divided into five groups receiving the treatments of vehicle (DMSO), an autophagy inducer rapamycin (1 mg/kg/day, i...
2017: International Journal of Biological Sciences
https://www.readbyqxmd.com/read/28362400/minimally-invasive-transverse-aortic-constriction-in-mice
#20
Aung Moe Zaw, Connor M Williams, Helen K W Law, Billy Kwok Chong Chow
Minimally invasive transverse aortic constriction (MTAC) is a more desirable method for the constriction of the transverse aorta in mice than standard open-chest transverse aortic constriction (TAC). Although transverse aortic constriction is a highly functional method for the induction of high pressure in the left ventricle, it is a more difficult and lengthy procedure due to its use of artificial ventilation with tracheal intubation. TAC is oftentimes also less survivable, as the newer method, MTAC, neither requires the cutting of the ribs and intercostal muscles nor tracheal intubation with a ventilation setup...
March 14, 2017: Journal of Visualized Experiments: JoVE
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