Characterization of a rat model of right-sided heart failure induced by pulmonary trunk banding

Schou, Uffe K.; Peters, Christian Daugaard; Kim, Soo Wan; Frøkiær, Jørgen; Nielsén, Sören

doi:10.1016/j.jeas.2006.10.004

Cited by 17 publications

(25 citation statements)

References 39 publications

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“…Another approach to induce high RVSBP and to increase right ventricular weight is by PTB [17], [20]. By comparing these two animal models, it is possible to distinguish the isolated effect of respectively pressure load and hypoxia.…”

Section: Discussionmentioning

confidence: 99%

Pressure Load: The Main Factor for Altered Gene Expression in Right Ventricular Hypertrophy in Chronic Hypoxic Rats

et al. 2011

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BackgroundThe present study investigated whether changes in gene expression in the right ventricle following pulmonary hypertension can be attributed to hypoxia or pressure loading.Methodology/Principal FindingsTo distinguish hypoxia from pressure-induced alterations, a group of rats underwent banding of the pulmonary trunk (PTB), sham operation, or the rats were exposed to normoxia or chronic, hypobaric hypoxia. Pressure measurements were performed and the right ventricle was analyzed by Affymetrix GeneChip, and selected genes were confirmed by quantitative PCR and immunoblotting. Right ventricular systolic blood pressure and right ventricle to body weight ratio were elevated in the PTB and the hypoxic rats. Expression of the same 172 genes was altered in the chronic hypoxic and PTB rats. Thus, gene expression of enzymes participating in fatty acid oxidation and the glycerol channel were downregulated. mRNA expression of aquaporin 7 was downregulated, but this was not the case for the protein expression. In contrast, monoamine oxidase A and tissue transglutaminase were upregulated both at gene and protein levels. 11 genes (e.g. insulin-like growth factor binding protein) were upregulated in the PTB experiment and downregulated in the hypoxic experiment, and 3 genes (e.g. c-kit tyrosine kinase) were downregulated in the PTB and upregulated in the hypoxic experiment.Conclusion/SignificancePressure load of the right ventricle induces a marked shift in the gene expression, which in case of the metabolic genes appears compensated at the protein level, while both expression of genes and proteins of importance for myocardial function and remodelling are altered by the increased pressure load of the right ventricle. These findings imply that treatment of pulmonary hypertension should also aim at reducing right ventricular pressure.

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Section: Discussionmentioning

confidence: 99%

Pressure Load: The Main Factor for Altered Gene Expression in Right Ventricular Hypertrophy in Chronic Hypoxic Rats

et al. 2011

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“…This might suggest that impaired RV function could translate to impaired LV function. In the rat model of right-sided heart failure produced by narrowing of the pulmonary artery, hypertrophy of the left ventricle and septum was observed as well as impairment of left ventricular function (Schou et al, 2007). However, LV function as assessed by peak systolic LVP increased.…”

Section: Functional Remodeling Of the Ventriclementioning

confidence: 96%

“…Recent studies suggested that there is a relationship between the two ventricles since they share the interventricular septum (Hill & Singal, 1997;Voelkel et al, 2006;Yu et al, 1996). Therefore, impairment of the right ventricular function may affect the function of the left ventricle (Schou, Peters, Kim, Frokiaer, & Nielsen, 2007). This might suggest that impaired RV function could translate to impaired LV function.…”

Section: Functional Remodeling Of the Ventriclementioning

confidence: 99%

“…Therefore, there is a need for an animal model of right ventricular hypertrophy. Several methods have been used to induce right ventricular hypertrophy including monocrotaline-induced vasculitis, hypoxia, and PAB (Bonnet et al, 2004;Jones et al, 2004;Schou et al, 2007). Among these models, PAB is an encouraging method for producing RVH and right-sided HF.…”

Section: Importance Of the Model And Translational To Humansmentioning

confidence: 99%

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Transmural dispersion of repolarization and cardiac remodeling in ventricles of rabbit with right ventricular hypertrophy

Meedech¹,

Saengklub²,

Limprasutr³

et al. 2015

Journal of Pharmacological and Toxicological Methods

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“…2,7 The rats were placed on a heating pad during the procedure to maintain body temperature at 37˚C. The pulmonary trunk was accessed through a thoracotomy on the left side of the sternum.…”

Section: Pulmonary Trunk Bandingmentioning

confidence: 99%

Acute Effects of Sildenafil and Dobutamine in the Hypertrophic and Failing Right Heart in Vivo

et al. 2013

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The purpose of this study was to investigate whether acute intravenous administration of the phosphodiesterase type 5 (PDE-5) inhibitor sildenafil in a single clinically relevant dose improves the in vivo function of the hypertrophic and failing right ventricle (RV). Wistar rats (n ¼ 24) were subjected to pulmonary trunk banding (PTB) causing RV hypertrophy and failure. Four weeks after surgery, they were randomized to receive an intravenous bolus dose of sildenafil (1 mg/kg; n ¼ 7), vehicle (n ¼ 6), or dobutamine (10 μg/kg; n ¼ 6 ). Invasive RV pressures were recorded continuously, and transthoracic echocardiography was performed 1,5,15,25, 35, 50, 70, and 90 minutes after injecting the bolus. Cardiac function was compared to baseline measurements to evaluate the in vivo effects of each specific treatment. The PTB procedure caused significant hypertrophy, cardiac fibrosis, and reduction in RV function evaluated by echocardiography (TAPSE) and invasive pressure measurements. Sildenafil did not improve the function of the hypertrophic failing right heart in vivo, measured by TAPSE, RV systolic pressure (RVsP), and dp/dt max . Dobutamine improved RV function 1 minute after injection measured by TAPSE (0:1242 AE 0:03 vs. 0:1565 AE 0:04 cm; P < 0:001 ), RVsP (83 AE 11 vs. 107 AE 11 mmHg; P < 0:001 ), and dp/dt max (3; 136 AE 521 vs. 4; 489 AE 706 mmHg/s; P < 0:001). Acute administration of the PDE-5 inhibitor sildenafil in a single clinically relevant dose did not modulate the in vivo function of the hypertrophic failing right heart of the rat measured by echocardiography and invasive hemodynamics. In the same model, dobutamine acutely improved RV function.

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Characterization of a rat model of right-sided heart failure induced by pulmonary trunk banding

Cited by 17 publications

References 39 publications

Pressure Load: The Main Factor for Altered Gene Expression in Right Ventricular Hypertrophy in Chronic Hypoxic Rats

Pressure Load: The Main Factor for Altered Gene Expression in Right Ventricular Hypertrophy in Chronic Hypoxic Rats

Transmural dispersion of repolarization and cardiac remodeling in ventricles of rabbit with right ventricular hypertrophy

Acute Effects of Sildenafil and Dobutamine in the Hypertrophic and Failing Right Heart in Vivo

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