Characterization of cardiac hypertrophy and heart  failure due to volume overload in the rat

Wang, Xi; Ren, Bin; Liu, Song-Yan; Sentex, Emmanuelle; Tappia, Paramjit S.; Dhalla, Naranjan S.

doi:10.1152/japplphysiol.00248.2002

Cited by 104 publications

(135 citation statements)

References 46 publications

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“…It was reported that the slope of the V O 2 -PVA relation was related to the ratio of the myosin isoform component from predominantly V3 to predominantly V1 (i.e., the slope of the V O 2 -PVA relation increases when the V1-to-V3 ratio increases, and the slope of the V O 2 -PVA relation is unchanged when the V1-to-V3 ratio decreases) (6). It was also reported that a progressive decrease in V1 and an increase in V3 were apparent in the LV 8-to 16 wk after AV shunt (21). This report is consistent with the almost unchanged slope of the V O 2 -PVA relation in the VO rats.…”

Section: Chemomechanical Energy Transductionmentioning

confidence: 95%

Mechanical work and energetic analysis of eccentric cardiac remodeling in a volume overload heart failure in rats

Takewa

Chemaly²,

Takaki³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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Eccentric cardiac remodeling seen in dilated cardiomyopathy or regurgitant valvular disease is a well-known process of heart failure progression, but its mechanoenergetic profile has not been yet established. We made a volume overload (VO) heart failure model in rats and for the first time investigated left ventricular (LV) mechanical work and energetics in cross-circulated whole heart preparations. Laparotomy was performed in 14 Wistar male rats, and abdominal aortic-inferior vena caval shunt was created in seven rats (VO group). Another seven rats underwent a sham operation without functional shunt (Sham group). LV dimensions changes were followed with weekly transthoracic echocardiography. Three months after surgery, we measured LV pressure and volume and myocardial O2 consumption in isolated heart cross circulation. LV internal dimensions in both systolic and diastolic phases were significantly increased in the VO group versus the Sham group (P Ͻ 0.05). LV pressure was markedly decreased in the VO group versus in the Sham group (P Ͻ 0.05). LV end-systolic pressurevolume relation shifted downward, and myocardial O2 consumption related to Ca 2ϩ handling significantly decreased. The contractile response to Ca 2ϩ infusion was attenuated. Nevertheless, the increase in Ca 2ϩ handling-related O2 consumption per unit change in LV contractility in the VO group was significantly higher than that in the Sham group (P Ͻ 0.05). The levels of sarco(endo)plasmic reticulum Ca 2ϩ -ATPase 2a protein were reduced in the VO group (P Ͻ 0.01). In conclusion, VO failing rat hearts had a character of marked contractile dysfunction accompanied with less efficient energy utilization in the Ca 2ϩ handling processes. These results suggest that restoring Ca 2ϩ handling in excitation-contraction coupling would improve the contractility of the myocardium after eccentric cardiac remodeling. eccentric left ventricular hypertrophy; myocardial oxygen consumption; Ca 2ϩ handling; sarco(endo)plasmic reticulum Ca 2ϩ -ATPase 2a; cross circulation; aortocaval shunt HEART FAILURE IS A MAJOR CAUSE of mortality and morbidity. It is due to various diseases such as hypertension, ischemic heart disease, valvular heart disease, congenital heart disease, cardiomyopathy, myocarditis, and others. The heart is subject to excessive and/or long-term overload, which induces myocardial hypertrophy. Hypertrophy initially compensates cardiac function but finally leads to heart failure. The process of hypertrophy and heart failure progression is divided into two mechanisms, depending on the type of overload: pressure overloading (PO) and volume overloading (VO). PO induces concentric hypertrophy to normalize wall stress from the increase in pressure placed on cardiomyocytes. Concentric remodeling of the left ventricle (LV) is characterized by an increase in ventricular wall thickness due to vertical growing of cardiomyocytes, which is caused by the parallel addition of sarcomeres (8).Conversely, VO promotes eccentric hypertrophy to compensate for excess blood volum...

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Section: Chemomechanical Energy Transductionmentioning

confidence: 95%

Mechanical work and energetic analysis of eccentric cardiac remodeling in a volume overload heart failure in rats

Takewa

Chemaly²,

Takaki³

et al. 2009

American Journal of Physiology-Heart and Circulatory Physiology

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“…In rats, significant cardiac hypertrophy develops 4 weeks after shunt induction, with compromised LV contractility and increased end-diastolic pressure [256]. Severe volume overload from a large aortocaval fistula initially leads to depressed LV function followed by a compensatory hypertrophy and near normal function at 4 weeks [165,307]. Decompensated hypertrophy or CHF develops between 8 and 16 weeks after the intervention and is characterized by a decline in systolic and diastolic function [34,308] and a shift between myosin heavy chain isoforms expression [307].…”

Section: Volume-overload-induced Hfmentioning

confidence: 99%

“…Severe volume overload from a large aortocaval fistula initially leads to depressed LV function followed by a compensatory hypertrophy and near normal function at 4 weeks [165,307]. Decompensated hypertrophy or CHF develops between 8 and 16 weeks after the intervention and is characterized by a decline in systolic and diastolic function [34,308] and a shift between myosin heavy chain isoforms expression [307]. Nonetheless, shunt closure has been reported in 7% of the cases, which means that it is necessary to confirm the patency of the shunt at the end of investigation.…”

Section: Volume-overload-induced Hfmentioning

confidence: 99%

Rodent models of heart failure: an updated review

et al. 2012

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Heart failure (HF) is one of the major health and economic burdens worldwide, and its prevalence is continuously increasing. The study of HF requires reliable animal models to study the chronic changes and pharmacologic interventions in myocardial structure and function and to follow its progression toward HF. Indeed, during the past 40 years, basic and translational scientists have used small animal models to understand the pathophysiology of HF and find more efficient ways of preventing and managing patients suffering from congestive HF (CHF). Each species and each animal model has advantages and disadvantages, and the choice of one model over another should take them into account for a good experimental design. The aim of this review is to describe and highlight the advantages and drawbacks of some commonly used HF rodents models, including both non-genetically and genetically engineered models, with a specific subchapter concerning diastolic HF models.

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“…Therefore, it is important to determine the mechanism responsible for volume overloadinduced ventricular remodeling. In this study, we created a volume overload rat model by abdominal artery-inferior vena cava puncture [25] . The Qp/Qs ratios in the remaining shunt rats were close to 2.0, suggesting successful creation of shunts and sustained volume overload.…”

Section: Discussionmentioning

confidence: 99%

Hydrogen sulfide suppresses the expression of MMP-8, MMP-13, and TIMP-1 in left ventricles of rats with cardiac volume overload

Zhang

et al. 2013

Acta Pharmacol Sin

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Aim: To study the effects of hydrogen sulfide (H 2 S) on the left ventricular expression of MMP-8, MMP-13, and TIMP-1 in a rat model of congenital heart disease. Methods: Male SD rats underwent abdominal aorta-inferior vena cava shunt operation. H 2 S donor NaHS (56 μmol·kg -1 ·d -1, ip) was injected from the next day for 8 weeks. At 8 weeks, the hemodynamic parameters, including the left ventricular systolic pressure (LVSP), the left ventricular peak rate of contraction and relaxation (LV±dp/dt max ) and the left ventricular end diastolic pressure (LVEDP) were measured. The left ventricular tissues were dissected out, and hydroxyproline and collagen I contents were detected with ELISA. The expression of MMP-8, MMP-13, and a tissue inhibitor of metalloproteinase-1 (TIMP-1) in the tissues was measured using real-time PCR, Western blotting, and immunohistochemistry, respectively. Results: The shunt operation markedly reduced LVSP and LV±dp/dt max , increased LVEDP, hydroxyproline and collagen I contents, as well as the mRNA and protein levels of MMP-8, MMP-13, and TIMP-1 in the left ventricles. Chronic treatment of the shunt operation rats with NaHS effectively prevented the abnormalities in the hemodynamic parameters, hydroxyproline and collagen I contents, and the mRNA and protein levels of MMP-13 and TIMP-1 in the left ventricles. NaHS also prevented the increase of MMP-8 protein expression, but did not affect the increase of mRNA level of MMP-8 in the shunt operation rats. Conclusion: H 2 S suppresses protein and mRNA expression of MMP-8, MMP-13, and TIMP-1 in rats with cardiac volume overload, which may be contributed to the amelioration of ventricular structural remodeling and cardiac function.

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Characterization of cardiac hypertrophy and heart failure due to volume overload in the rat

Cited by 104 publications

References 46 publications

Mechanical work and energetic analysis of eccentric cardiac remodeling in a volume overload heart failure in rats

Mechanical work and energetic analysis of eccentric cardiac remodeling in a volume overload heart failure in rats

Rodent models of heart failure: an updated review

Hydrogen sulfide suppresses the expression of MMP-8, MMP-13, and TIMP-1 in left ventricles of rats with cardiac volume overload

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