Összesen 3 találat.


001-es BibID:BIBFORM015750
Első szerző:Machackova, Jarmila
Cím:Amelioration of Cardiac Remodeling in Congestive Heart Failure by beta-Adrenoceptor Blockade is Associated with Depression in Sympathetic Activity / Jarmila Machackova, Santosh K. Sanganalmath, Barta Judit, Ken S. Dhalla, Naranjan S. Dhalla
Megjegyzések:This study investigated whether improvement in cardiac function and attenuation of cardiac remodeling by some b-adrenoceptor (b-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. Sham-operated rats served as controls. Both atenolol and propranolol at 20 and 75 mg/kg doses attenuated the MI-induced cardiac hypertrophy, increases in left ventricular (LV) end-diastolic pressure, LV end-systolic volume and LV end-diastolic volume as well as depressions in LV systolic pressure, LV fractional shortening and cardiac output. PR interval was decreased and QTc interval was increased in CHF; these alterations were ameliorated by both atenolol and propranolol. The increased level of plasma epinephrine in CHF was also depressed by both low and high doses of atenolol and propranolol whereas the increased level of plasma norepinephrine was reduced by high but not low doses of these drugs. The results indicate that the beneficial effects of b-AR antagonists on cardiacremodeling and heart dysfunction in CHF may be due tothe blockade of b-ARs in the myocardium and a depressionin the sympathetic activity.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cardiac dysfunction
Plasma catecholamines
beta-Adrenoceptor antagonists
Cardiac hypertrophy and failure
Megjelenés:Cardiovascular Toxicology. - 10 : 1 (2010), p. 9-16. -
További szerzők:Sanganalmath, Santosh K. Barta Judit (1975-) (kardiológus) Dhalla, Ken S. Dhalla, Naranjan S.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat


001-es BibID:BIBFORM015746
Első szerző:Machackova, Jarmila
Cím:Myofibrillar remodelling in cardiac hypertrophy, heart failure and cardiomyopathies / Jarmila Machackova, Barta Judit, Naranjan S. Dhalla
Megjegyzések:A wide variety of pathological conditions havebeen 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 asin signal transduction and metabolism in the heart, among different cardiovascular disorders. The present review is focused on identifying the alterations in molecular and biochemical structure of myofibrils (myofibrillar remodelling) in hypertrophied and failing myocardiumin different types of heart diseases. Numerous changes at the level of gene expression for both contractile and regulatory proteins have already been reported in failing hearts and heart diseases; these changes are potential precursors for heart failure such as cardiac hypertrophyand cardiomyopathies. Myofibrillar remodelling, as a consequence of proteolysis, oxidation, and phosphorylation of some functional groups in both contractile and regulatory proteins in hearts failing due to different etiologies, has also been described. CONCLUSIONS: Although myofibrillar remodelling appears to be associated with cardiac dysfunction, alterations in both contractileand regulatory proteins are dependent on the type and stage of heart disease.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Cardiac gene expression
Congestive heart failure
Myocardial infarction
Myofibrillar alterations
Megjelenés:The Canadian Journal of Cardiology. - 22 : 11 (2006), p. 953-968. -
További szerzők:Barta Judit (1975-) (kardiológus) Dhalla, Naranjan S.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat


001-es BibID:BIBFORM015745
Első szerző:Machackova, Jarmila
Cím:Molecular defects in cardiac myofibrillar proteins due to thyroid hormone imbalance and diabetes / Jarmila Machackova, Barta Judit, Naranjan S. Dhalla
Megjegyzések:The heart very often becomes a victim of endocrine abnormalities such as thyroid hormone imbalance and insulindeficiency, which are manifested in a broad spectrum of cardiac dysfunction from mildly compromised function tosevere 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. Changes in the contractile and regulatory proteins constitute molecular and structural alterations in myofibrillar assembly, called myofibrillar remodeling.These alterations may be adaptive or maladaptive with respect to the functional and metabolic demands on the heart as a consequence of the altered endocrine status in the body. There is a substantial body of information to indicate alterations in myofibrillar proteins including actin, myosin, tropomyosin, troponin, titin, desmin, and myosin-binding protein C in conditions such as hyperthyroidism, hypothyroidism, and diabetes. The present article is focussed on discussion how myofibrillar proteins are altered in response to thyroid hormone imbalance and lack of insulin or its responsiveness, and how their structural and functional changes explain the contractile defects in the heart.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
diabetic cardiomyopathy
insulin deficiency
insulin resistance
myofibrillar remodeling
Megjelenés:Canadian Journal of Physiology and Pharmacology 83 : 12 (2005), p. 1071-1091. -
További szerzők:Barta Judit (1975-) (kardiológus) Dhalla, Naranjan S.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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