β-adrenergic blockade attenuates cardiac dysfunction and myofibrillar remodelling in congestive heart failure.

Although β-adrenoceptor (β-AR) blockade is an important mode of therapy for congestive heart failure (CHF), subcellular mechanisms associated with its beneficial effects are not clear. Three weeks after inducing myocardial infarction (MI), rats were treated daily with or without 20 and 75 mg/kg atenolol, a selective β(1) -AR antagonist, or propranolol, a non-selective β-AR antagonist, for 5 weeks. Sham operated rats served as controls.

Amelioration of cardiac remodeling in congestive heart failure by beta-adrenoceptor blockade is associated with depression in sympathetic activity.

This study investigated whether improvement in cardiac function and attenuation of cardiac remodeling by some beta-adrenoceptor (beta-AR) antagonists were associated with a depression in sympathetic activity in congestive heart failure (CHF) due to myocardial infarction (MI). Although cardiac dysfunction, hypertrophy and dilatation as well as increased plasma level of catecholamines are known to occur in CHF, the relationship between these parameters is poorly understood. Three weeks after occlusion of the coronary artery, rats were treated daily with 20 and 75 mg/kg of either atenolol or propranolol for 5 weeks.

Myofibrillar remodeling in cardiac hypertrophy, heart failure and cardiomyopathies.

Background: A wide variety of pathological conditions have been shown to result in cardiac remodelling and myocardial dysfunction. However, the mechanisms of transition from adaptive to maladaptive alterations, as well as those for changes in cardiac performance leading to heart failure, are poorly understood.

Observations: Extensive studies have revealed a broad spectrum of progressive changes in subcellular structures and function, as well as in signal transduction and metabolism in the heart, among different cardiovascular disorders.

Molecular defects in cardiac myofibrillar proteins due to thyroid hormone imbalance and diabetes.

The heart very often becomes a victim of endocrine abnormalities such as thyroid hormone imbalance and insulin deficiency, which are manifested in a broad spectrum of cardiac dysfunction from mildly compromised function to severe heart failure. These functional changes in the heart are largely independent of alterations in the coronary arteries and instead reside at the level of cardiomyocytes. The status of cardiac function reflects the net of underlying subcellular modifications induced by an increase or decrease in thyroid hormone and insulin plasma levels.

Renin-angiotensin blockade attenuates cardiac myofibrillar remodelling in chronic diabetes.

Previous studies have shown that the renin-angiotensin system (RAS) is activated in diabetes and this may contribute to the subcellular remodelling and heart dysfunction in this disease. Therefore, we examined the effects of RAS blockade by enalapril, an angiotensin-converting enzyme inhibitor, and losartan, an angiotensin receptor AT1 antagonist, on cardiac function, myofibrillar and myosin ATPase activity as well as myosin heavy chain (MHC) isozyme expression in diabetic hearts. Diabetes was induced in rats by a single injection of streptozotocin (65 mg/kg; i.

Role of reactive oxygen species in ischemic preconditioning of subcellular organelles in the heart.

Ischemic preconditioning (IPC) is an endogenous adaptive mechanism and is manifested by early and delayed phases of cardioprotection. Brief episodes of ischemia-reperfusion during IPC cause some subtle functional and structural alterations in sarcolemma, mitochondria, sarcoplasmic reticulum, myofibrils, glycocalyx, as well as nucleus, which render these subcellular organelles resistant to subsequent sustained ischemia-reperfusion insult. These changes occur in functional groups of various receptors, cation transporters, cation channels, and contractile and other proteins, and may explain the initial effects of IPC.

Effect of sodium 2,3-dimercaptopropane-1-sulphonate (DMPS) on chronic daunorubicin toxicity in rabbits: comparison with dexrazoxane.

A possible protective action of DMPS (a dithiol chelating agent) against chronic daunorubicin toxicity in rabbits in comparison with dexrazoxane was investigated. The rabbits were divided into five groups: control (saline, 1 ml/kg i.v.

Troponins in experimental studies.

The aim of our study was to compare the diagnostic performance of cardiac troponin T (cTnT) and cardiac troponin I (cTnI) in three groups of rabbits: 1) control (saline 1 ml/kg i.v.); 2) daunorubicin (3 mg/kg i.