Experimental Models of Heart Failure and Cardiomyopathy

1996 ◽  
pp. 3-8
Author(s):  
Gordon W. Moe ◽  
Paul W. Armstrong
Keyword(s):  
Heart Failure ◽  
Experimental Models

scholarly journals Effects of Beraprost Sodium in experimental models of heart failure.

1996 ◽  
Vol 71 ◽  
pp. 320
Author(s):  
Hiroki Kumagai ◽  
Masafumi Isogaya ◽  
Seiji Okazaki ◽  
Shintaro Nishio
Keyword(s):  
Heart Failure ◽  
Experimental Models ◽  
Beraprost Sodium

Peripheral chemoreceptors in health and disease

2004 ◽  
Vol 96 (1) ◽  
pp. 359-366 ◽  
Author(s):  
Nanduri R. Prabhakar ◽  
Ying-Jie Peng
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Defense Mechanism ◽  
Experimental Models ◽  
Cellular Mechanisms ◽  
Peripheral Chemoreceptor ◽  
Peripheral Chemoreceptors ◽  
Oxygen Homeostasis ◽  
Arterial Blood ◽  
Carotid Bodies

Peripheral chemoreceptors (carotid and aortic bodies) detect changes in arterial blood oxygen and initiate reflexes that are important for maintaining homeostasis during hypoxemia. This mini-review summarizes the importance of peripheral chemoreceptor reflexes in various physiological and pathophysiological conditions. Carotid bodies are important for eliciting hypoxic ventilatory stimulation in humans and in experimental animals. In the absence of carotid bodies, compensatory upregulation of aortic bodies as well as other chemoreceptors contributes to the hypoxic ventilatory response. Peripheral chemoreceptors are critical for ventilatory acclimatization at high altitude. They also contribute in part to the exercise-induced hyperventilation, especially with submaximal and heavy exercise. During pregnancy, hypoxic ventilatory sensitivity increases, perhaps due to the actions of estrogen and progesterone on chemoreceptors. Augmented peripheral chemoreceptors have been implicated in early stages of recurrent apneas, congestive heart failure, and certain forms of hypertension. It is likely that chemoreceptors tend to maintain oxygen homeostasis and act as a defense mechanism to prevent the progression of the morbidity associated with these diseases. Experimental models of recurrent apneas, congestive heart failure, and hypertension offer excellent opportunities to unravel the cellular mechanisms associated with altered chemoreceptor function.

Pulmonary Edema I: Cardiogenic Pulmonary Edema

2017 ◽  
Author(s):  
Annette Esper ◽  
Greg S Martin ◽  
Gerald W. Staton Jr
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Pulmonary Edema ◽  
Clinical Characteristics ◽  
Distress Syndrome ◽  
Capillary Permeability ◽  
Treatment Options ◽  
Experimental Models ◽  
Lung Mechanics ◽  
Cardiogenic Pulmonary Edema

There are two categories of pulmonary edema: edema caused by increased capillary pressure (hydrostatic or cardiogenic edema) and edema caused by increased capillary permeability (noncardiogenic pulmonary edema, or acute respiratory distress syndrome). This review focuses on cardiogenic pulmonary edema and describes the general approach to patients with suspected cardiogenic pulmonary edema. The pathogenesis, diagnosis, treatment, and outcome of cardiogenic pulmonary edema are reviewed. Figures include chest scans showing pulmonary edema and noncardiogenic pulmonary edema, an illustration of the differences between cardiogenic and noncardiogenic edema, and a chart comparing lung mechanics and other variables in experimental models of cardiogenic pulmonary edema and noncardiogenic edema. Tables show clinical characteristics of patients with cardiogenic pulmonary edema and treatment options. This review contains 3 figures, 4 tables, and 24 references. Key words: cardiogenic pulmonary edema, congestive heart failure, pulmonary edema, Starling’s law

Congestive Heart Failure in Copper-Deficient Mice

2003 ◽  
Vol 228 (7) ◽  
pp. 811-817 ◽  
Author(s):  
Laila Elsherif ◽  
Raymond V. Ortines ◽  
Jack T. Saari ◽  
Y. James Kang
Keyword(s):  
Heart Failure ◽  
Congestive Heart Failure ◽  
Left Ventricle ◽  
Diastolic Pressure ◽  
Systolic Pressure ◽  
Pressure Rise ◽  
Experimental Models ◽  
Left Ventricular ◽  
Mouse Heart ◽  
Total Period

Copper Deficiency (CuD) leads to hypertrophic cardiomyopathy in various experimental models. The morphological, electrophysiological, and molecular aspects of this hypertrophy have been under investigation for a long time. However the transition from compensated hypertrophy to decompensated heart failure has not been investigated in the study of CuD. We set out to investigate the contractile and hemodynamic parameters of the CuD mouse heart and to determine whether heart failure follows hypertrophy in the CuD heart. Dams of FVB mice were fed CuD or copper-adequate (CuA) diet starting from the third day post delivery and the weanling pups were fed the same diet for a total period of 5 weeks (pre- and postweanling). At week 4, the functional parameters of the heart were analyzed using a surgical technique for catheterizing the left ventricle. A significant decrease in left ventricle systolic pressure was observed with no significant change in heart rate, and more importantly contractility as measured by the maximal rate of left ventricular pressure rise (+dP/dt) and decline (−dP/dt) were significantly depressed in the CuD mice. However, left ventricle end diastolic pressure was elevated, and relaxation was impaired in the CuD animals; the duration of relaxation was prolonged. In addition to significant changes in the basal level of cardiac function, CuD hearts had a blunted response to the stimulation of the β-adrenergic agonist isoproterenol. Furthermore, morphological analysis revealed increased collagen accumulation in the CuD hearts along with lipid deposition. This study shows that CuD leads to systolic and diastolic dysfunction in association with histopathological changes, which are indices commonly used to diagnose congestive heart failure.

scholarly journals Diabetic cardiomyopathy

2009 ◽  
Vol 116 (10) ◽  
pp. 741-760 ◽  
Author(s):  
Omar Asghar ◽  
Ahmed Al-Sunni ◽  
Kaivan Khavandi ◽  
Ali Khavandi ◽  
Sarah Withers ◽  
...  
Keyword(s):  
Heart Failure ◽  
Diabetic Cardiomyopathy ◽  
Disease Process ◽  
Molecular Targets ◽  
Clinical Trial Data ◽  
Experimental Models ◽  
Trial Data ◽  
Diabetic Patients ◽  
Cardiac Safety ◽  
Artery Disease

Diabetic cardiomyopathy is a distinct primary disease process, independent of coronary artery disease, which leads to heart failure in diabetic patients. Epidemiological and clinical trial data have confirmed the greater incidence and prevalence of heart failure in diabetes. Novel echocardiographic and MR (magnetic resonance) techniques have enabled a more accurate means of phenotyping diabetic cardiomyopathy. Experimental models of diabetes have provided a range of novel molecular targets for this condition, but none have been substantiated in humans. Similarly, although ultrastructural pathology of the microvessels and cardiomyocytes is well described in animal models, studies in humans are small and limited to light microscopy. With regard to treatment, recent data with thiazoledinediones has generated much controversy in terms of the cardiac safety of both these and other drugs currently in use and under development. Clinical trials are urgently required to establish the efficacy of currently available agents for heart failure, as well as novel therapies in patients specifically with diabetic cardiomyopathy.

The Forgotten Driving Forces in Right Heart Failure: New Concept and Device

2009 ◽  
Vol 17 (5) ◽  
pp. 525-530 ◽  
Author(s):  
Sayed Nour ◽  
Guifu Wu ◽  
Zheng Zhensheng ◽  
Juan C Chachques ◽  
Alain Carpentier ◽  
...  
Keyword(s):  
Heart Failure ◽  
Right Ventricular ◽  
Driving Forces ◽  
Right Heart Failure ◽  
Experimental Models ◽  
Right Heart ◽  
Assist Device ◽  
Venous Capacitance ◽  
Non Invasive ◽  
The Right

Background: Right heart failure is a frequent hemodynamic disturbance in pediatric cardiac patients. Besides inotropic and chronotropic drugs, fluid administration and inhaled nitric oxide, right ventricular mechanical assistance remains difficult to perform. A circulatory assist device adapted for the right heart biophysics and physiology might be more efficient. Materials and Methods: We are developing a prototype of a non-invasive cardiac assist device (CAD) for neonates and pediatrics. It is based on a pulsatile suit device covering and affecting all territories of the right heart circuit. It will be tested in a neonatal animal model of right ventricular (RV) failure. Experimental models will be matched and compared with control and sham groups. Expected results would be immediate hemodynamic improvement due to synchronized diastolic reduction of stagnant venous capacitance, increasing preload and contractility. On long term, increased shear stress with changing intrathoracic pressure in a phasic way would improve and remodel the pulmonary circulation. Future studies will be focused on: hemodynamic, biochemistry, endothelium function test, and angiogenesis. Comments: A non-invasive CAD guarantees better hemodynamics and endothelial function preservation with low morbidity and mortality. This is a physiological approach, cost-effective method, and particularly interesting in neonates and pediatrics with RV failure.

scholarly journals Hepatic Clearance of Renin in Canine Experimental Models for Low- and High-Output Heart Failure

1969 ◽  
Vol 24 (2) ◽  
pp. 213-219 ◽  
Author(s):  
EDWARD G. SCHNEIDER ◽  
James O. Davis ◽  
Charles A. ROBB ◽  
John S. Baumber
Keyword(s):  
Heart Failure ◽  
Hepatic Clearance ◽  
Experimental Models ◽  
High Output Heart Failure ◽  
High Output

Experimental models for investigating the pathogenesis of heart failure

2022 ◽  
pp. 103-122
Author(s):  
Sukhwinder K. Bhullar ◽  
Naranjan S. Dhalla
Keyword(s):  
Heart Failure ◽  
Experimental Models

Heart failure due to chronic experimental aortic regurgitation

1994 ◽  
Vol 267 (2) ◽  
pp. H556-H562 ◽  
Author(s):  
N. M. Magid ◽  
G. Opio ◽  
D. C. Wallerson ◽  
M. S. Young ◽  
J. S. Borer
Keyword(s):  
Heart Failure ◽  
Aortic Regurgitation ◽  
Systolic Dysfunction ◽  
Disease Process ◽  
Experimental Models ◽  
Left Ventricular ◽  
Sham Operation ◽  
Systolic Performance ◽  
Baseline Values ◽  
Chronic Aortic Regurgitation

Previously reported experimental models of aortic regurgitation generally have manifested normal systolic performance and have not developed heart failure [Magid et al. Am. J. Physiol. 263 (Heart Circ. Physiol. 32): H226–H233, 1992]. To determine whether more severe chronic experimental aortic regurgitation would generate systolic malperformance, heart failure, and emulate the human disease process, 11 New Zealand White rabbits underwent surgical induction of aortic regurgitation and 5 control animals underwent sham operation. Doppler echocardiography was performed serially for up to 3 yr, and pathological studies were performed at necropsy. Left ventricular internal dimension at end diastole increased 80% (P < 0.00002) and left ventricular weight increased 250% (P < 0.0002) in aortic regurgitant rabbits (regurgitant fraction 52 +/- 13%) compared with baseline values. Six of 11 aortic regurgitant animals died with pathological evidence of congestive heart failure at 1.5 +/- 0.8 yr postoperatively; 2 of these developed severe systolic malperformance, manifest as fractional shortenings of 15 and 19% at 1.6 and 1.7 yr, respectively. Five of 11 aortic regurgitant animals survived until killed at 2.9 +/- 0.1 yr. Thus moderate-to-severe chronic aortic regurgitation in rabbits frequently results in heart failure and systolic dysfunction and may usefully model chronic aortic regurgitation and heart failure in humans.

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