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Cited by 4 publications
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Ž .Heart failure HF is a common clinical problem confronting physicians and is often the final manifestation of many cardiovascular disorders. Despite recent advances in the pharmacological management of HF, it remains a highly lethal and disabling disorder. A number of animal models have been developed to study both the pathophysiology of HF and new therapeutic approaches to this complex syndrome. Only through an improved understanding of the basic biology of the early stages of the syndrome can HF be prevented or at least anticipated. With this in view, we have developed an easily realisable and inexpensive model in the guinea pig, which presents numerous structural, metabolic and biochemical similarities compared with the human heart. Thirty guinea pigs, aged 5 weeks and weighing 300 g were used. After anaesthesia, left Ž . Ž . nephrectomy was performed. After 1 week the guinea pigs were divided into: a control group n s 15 , which received an Ž . Ž . injection of vehicle as well as tap water for 10 weeks; b DOCA-salts group n s 15 , where the animals were treated with an IM injection of 10 mg DOCA 5 days a week for 10 weeks and with drinking water containing 9 grl y1 NaCl and 2 grl y1 KCl. Our results demonstrate that the administration of DOCA-salts to guinea pigs for 10 weeks caused a significant increase in Ž . Ž . Ž . blood pressure BP q 30% associated with left ventricular hypertrophy LVH , evaluated by LV weight q37% , LV wall Ž . Ž . Ž . q36% , by the ratio LV weightrBody weight q23% and by an increase in LV volume q51% . Concerning HF, the latter was clinically evident through an increase in body weight, heart rate and dyspnoea. Indeed, guinea pigs presented pleural andror pericardial effusion often associated with ascite. This model, which combines pressure and volume overload, results in a slow evolution towards HF. This allows a better understanding of the mechanisms in early LV remodelling which has the potential to develop into HF. Some recent studies have emphasised the value of using guinea pigs. The guinea pig heart muscle presents two major regulatory mechanisms of contractility that are closer to those found in humans, the isomyosin pattern which is predominantly V and the phenomenon of Ca 2q -induced Ca 2q -release from the sarcoplasmic reticulum. The 3 DOCA-salts model in the guinea pig is an easy surgical procedure with high post-operative survival, which causes an increase in arterial BP, LVH associated with HF. This model is a useful tool for studying some of the basic mechanisms of cardiovascular diseases. ᮊ
Ž .Heart failure HF is a common clinical problem confronting physicians and is often the final manifestation of many cardiovascular disorders. Despite recent advances in the pharmacological management of HF, it remains a highly lethal and disabling disorder. A number of animal models have been developed to study both the pathophysiology of HF and new therapeutic approaches to this complex syndrome. Only through an improved understanding of the basic biology of the early stages of the syndrome can HF be prevented or at least anticipated. With this in view, we have developed an easily realisable and inexpensive model in the guinea pig, which presents numerous structural, metabolic and biochemical similarities compared with the human heart. Thirty guinea pigs, aged 5 weeks and weighing 300 g were used. After anaesthesia, left Ž . Ž . nephrectomy was performed. After 1 week the guinea pigs were divided into: a control group n s 15 , which received an Ž . Ž . injection of vehicle as well as tap water for 10 weeks; b DOCA-salts group n s 15 , where the animals were treated with an IM injection of 10 mg DOCA 5 days a week for 10 weeks and with drinking water containing 9 grl y1 NaCl and 2 grl y1 KCl. Our results demonstrate that the administration of DOCA-salts to guinea pigs for 10 weeks caused a significant increase in Ž . Ž . Ž . blood pressure BP q 30% associated with left ventricular hypertrophy LVH , evaluated by LV weight q37% , LV wall Ž . Ž . Ž . q36% , by the ratio LV weightrBody weight q23% and by an increase in LV volume q51% . Concerning HF, the latter was clinically evident through an increase in body weight, heart rate and dyspnoea. Indeed, guinea pigs presented pleural andror pericardial effusion often associated with ascite. This model, which combines pressure and volume overload, results in a slow evolution towards HF. This allows a better understanding of the mechanisms in early LV remodelling which has the potential to develop into HF. Some recent studies have emphasised the value of using guinea pigs. The guinea pig heart muscle presents two major regulatory mechanisms of contractility that are closer to those found in humans, the isomyosin pattern which is predominantly V and the phenomenon of Ca 2q -induced Ca 2q -release from the sarcoplasmic reticulum. The 3 DOCA-salts model in the guinea pig is an easy surgical procedure with high post-operative survival, which causes an increase in arterial BP, LVH associated with HF. This model is a useful tool for studying some of the basic mechanisms of cardiovascular diseases. ᮊ
Background Regression of left ventricular hypertrophy (LVH) after surgical correction for aortic stenosis is not fully understood on the molecular level. The aim of this study was to examine whether there is an association between LVH regression and extracellular matrix (ECM) gene expression. Methods and Results A standard model of controlled LVH induction by supracoronary banding (A=baseline) was applied in 44 growing sheep (age, 6 to 8 months). Surgical correction to release the pressure gradient was performed 8.3±1 months later (B). The animals were killed after another 10.1±2 months (C). At all time points, hemodynamic evaluations and quantitative analysis of mRNA and protein expression for matrix metalloproteinases (MMP) and their tissue inhibitors (TIMP) was performed. Left ventricular mass index was 82±21 (A) versus 150±33 (B), P <0.01, and 78±18 g/m 2 (C), P <0.01. Left ventricular function and cardiac index remained stable. Myocardial fiber diameter index was 9.1±1.2 (A) versus 12.3±1.4 (B), P <0.01, and 8.4±1.3 μm/m 2 (C), P <0.01. In parallel to the development of LVH at B, gene expression was increased significantly for MMP-1, MMP-2, MMP-3, and MMP-9 and for TIMP-1 and TIMP-2 and decreased significantly for TIMP-3. After surgical correction (C), there was a complete regression of gene expression to baseline measures. Conclusions Controlled induction of compensated LVH leads to significant increase in ECM gene expression. The regression of LVH after surgical therapy is associated with complete regression of ECM gene expression. However, no cause-and-effect relation could be demonstrated.
Background-Left ventricular (LV) apical rotation and twist can be estimated noninvasively by speckle-tracking echocardiography (STE). In this study, we tested whether apical rotation is an accurate index of LV contractility. Methods and Results-We measured LV basal and apical rotation by STE in 11 open-chest anesthetized mongrel dogs under 8 different inotropic stages before and after ligation of either left anterior descending (nϭ6) or circumflex coronary artery (nϭ5). We measured LV pressure simultaneously with a high-fidelity pressure catheter and calculated LV ejection fraction (EF) with the biplane Simpson method and 2D echocardiography. Maximal positive dP/dt (dP/dt max ) was used as the gold standard measurement of LV contractility. We compared LV twist and apical rotation and EF against dP/dt max by linear mixed model. LV apical rotation and twist showed dose-dependent increases and decreases after dobutamine and esmolol infusion, respectively. However, basal rotation did not change significantly during different inotropic conditions. There was a stronger association between dP/dt max and LV twist (R 2 ϭ0.747, PϽ0.001) and apical rotation (R
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