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001-es BibID:	BIBFORM005624
Első szerző:	Barta Judit (kardiológus)
Cím:	Antiplatelet agents sarpogrelate and cilostazol affect experimentally-induced ventricular arrhythmias and mortality / Barta, J., Sanganalmath, S. K., Kumamoto, H., Takeda, N., Edes, I., Dhalla, N. S.
Dátum:	2008
ISSN:	1530-7905 (Print)
Megjegyzések:	Antiplatelet agents, sarpogrelate (SAR), a 5-hydroxy tryptamine 2A receptor antagonist and cilostazol (CIL), a phosphodiesterase-III inhibitor, were observed to be beneficial in attenuating cardiac remodeling and improving cardiac function in congestive heart failure due to myocardial infarction in rats; however, CIL increased ventricular tachycardia and mortality. In order to study the effects of these antiplatelet agents on arrhythmias, Sprague-Dawley rats were pretreated with either SAR or CIL (5 mg/kg/day) for 2 weeks and were then either injected cumulative doses of epinephrine (Epi) or subjected to coronary occlusion. Saline-treated animals served as controls. Electrocardiographic analysis revealed that SAR pretreatment decreased the incidence and severity of ventricular arrhythmias (time of onset of arrhythmias as well as the occurrence of premature ventricular contractions, salvos, tachycardia, and fibrillations), whereas CIL treatment augmented the incidence of cardiac arrhythmias due to both Epi and coronary occlusion. None of the drugs affected the corrected QT interval significantly. Furthermore, the levels of cyclic adenosine monophosphate (cAMP) in left ventricle were markedly higher in CIL-pretreated rats when compared to SAR-pretreated or control rats. It is suggested that an excessive level of cAMP may contribute to increase incidence of ventricular arrhythmias and mortality in animals pretreated with CIL, unlike the SAR-pretreated rats.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Anti-Arrhythmia Agents/pharmacology Arrhythmias, Cardiac/chemically induced/metabolism/prevention & control Coronary Occlusion/complications/drug therapy/metabolism Cyclic AMP/metabolism Disease Models, Animal Electrocardiography Epinephrine Heart Ventricles/drug effects/metabolism Male Platelet Aggregation Inhibitors/adverse effects/pharmacology Rats Rats, Sprague-Dawley Succinates/pharmacology Tetrazoles/*adverse effects Time Factors Up-Regulation
Megjelenés:	Cardiovasc Toxicology. - 8 : 3 (2008), p. 127-135. -
További szerzők:	Sanganalmath, Santosh K. Kumamoto, Hideo Takeda, Nobuakira Édes István (1952-) (kardiológus) Dhalla, Naranjan S.
Internet cím:	elektronikus változat elektronikus változat DOI
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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
Dátum:	2010
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 DOI
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001-es BibID:	BIBFORM005640
Első szerző:	Sanganalmath, Santosh K.
Cím:	Antiplatelet therapy attenuates subcellular remodelling in congestive heart failure / Sanganalmath, S. K., Babick, A. P., Barta, J., Kumamoto, H., Takeda, N., Dhalla, N. S.
Dátum:	2008
ISSN:	1582-1838 (Print)
Megjegyzések:	Antiplatelet agents, sarpogrelate (SAR), a 5-HT(2A) receptor antagonist, and cilostazol (CIL), a phosphodiesterase III (PDE-III) inhibitor, are used for the treatment of peripheral vascular disease. We tested whether these agents affect cardiac function and subcellular remodelling in congestive heart failure (CHF) induced by myocardial infarction (MI). Three weeks after MI, rats were treated daily with 5 mg/kg SAR or CIL as well as vehicle for 5 weeks. Sham-operated animals served as controls. At end of the treatment period, haemodynamic measurements were performed and the left ventricle was processed for the determination of sarcoplasmic reticulum (SR) Ca(2+)-uptake and -release activities, and expression of SR Ca(2+)-pump, phospholamban and ryanodine receptors, as well as myofibrillar ATPase activities, expression of alpha- and beta-myosin heavy chain (MHC) isoforms, and phosphorylation of phospholamban and cardiac troponin-I (c Tn-I). Marked haemodynamic changes in the MI-induced CHF were associated with depressions in SR Ca (+)-uptake and -release activities as well as in protein content and gene expression for SR proteins. Furthermore, myofibrillar Ca(2+)-stimulated ATPase activity, as well as protein content and gene expression for alpha-MHC were decreased whereas those for beta-MHC were increased in the failing heart. Also, phosphorylation levels of phospholamban and cTn-I were reduced in failing hearts. The MI-associated changes in cardiac function, SR and myofibillar activities, as well as SR and myofibrillar protein and gene expression were attenuated by treatment with SAR or CIL. The results suggest that SAR and CIL improve cardiac function by ameliorating subcellular remodelling in the failing heart and indicate the potential therapy of CHF with antiplatelet agents.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Adenosine Triphosphatases/metabolism Animals Blood Platelets Calcium/metabolism Gene Expression Regulation Heart Failure/genetics/metabolism/surgery/ therapy Hemodynamics Male Myosin Heavy Chains/metabolism Protein Isoforms/metabolism Proteins/genetics/metabolism RNA, Messenger/genetics Rats Rats, Sprague-Dawley Sarcoplasmic Reticulum/metabolism Subcellular Fractions/metabolism
Megjelenés:	Journal of Cellular and Molecular Medicine. - 12 : 5A (2008), p. 1728-1738. -
További szerzők:	Babick, Andrea P. Barta Judit (1975-) (kardiológus) Kumamoto, Hideo Takeda, Nobuakiya Dhalla, Naranjan S.
Internet cím:	DOI elektronikus változat
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001-es BibID:	BIBFORM005641
Első szerző:	Sanganalmath, Santosh K.
Cím:	Antiplatelet therapy mitigates cardiac remodeling and dysfunction in congestive heart failure due to myocardial infarction / Sanganalmath, S. K., Barta, J., Takeda, N., Kumamoto, H., Dhalla, N. S.
Dátum:	2008
ISSN:	0008-4212 (Print)
Megjegyzések:	Antiplatelet agents such as sarpogrelate (SAR), a 5-hydroxytryptamine antagonist, and cilostazol (CIL), a phosphodiesterase-III inhibitor, are used in the management of peripheral vascular disease. In this study, we tested the hypothesis that both SAR and CIL prevent cardiac remodeling and improve cardiac function in congestive heart failure (CHF) due to myocardial infarction (MI). Post-MI rats (3 weeks after the occlusion of coronary artery) received either vehicle (MI+V, n = 36), SAR (MI+SAR; 5 mg xc kg(-1) x day(-1), n = 35) or CIL (MI+CIL; 5 mg x kg(-1) x day(-1), n = 34) from day 21 to day 56. Sham-operated rats (n = 29) served as controls. Electrocardiographic, echocardiographic, and hemodynamic parameters were measured on day 56. Treatment of infarcted animals with SAR or CIL significantly improved the left ventricular (LV) dimensions, LV fractional shortening, cardiac output, stroke volume, mean arterial pressure, LV diastolic function, and LV systolic pressure, as well as rates of LV pressure development and pressure decay. Although cardiac hypertrophy was reduced, both SAR and CIL had no effect on infarct size or MI-associated QTc prolongation. However, SAR decreased whereas CIL increased the incidence of ventricular arrhythmias and the mean number of episodes in infarcted animals. Mortality during the treatment period was decreased by 17% with SAR and increased by 10% with CIL, but these changes were not significant statistically. The data in this study suggest that both SAR and CIL prevent cardiac remodeling and improve cardiac function in MI-induced CHF; however, CIL unlike SAR increased the incidence of arrhythmias and adversely affected patient mortality.
Tárgyszavak:	Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban Animals Arrhythmias Disease Models, Animal Echocardiography Electrocardiography Heart Failure Hemodynamics Male Myocardial Contraction Myocardial Infarction Platelet Aggregation Inhibitors Rats Rats, Sprague-Dawley Succinates Tetrazoles Time Factors Ventricular Dysfunction control Ventricular Remodeling
Megjelenés:	Canadian Journal of Physiology and Pharmacology. - 86 : 4 (2008), p. 180-189. -
További szerzők:	Barta Judit (1975-) (kardiológus) Takeda, Nobuakira Kumamoto, Hideo Dhalla, Naranjan S.
Internet cím:	elektronikus változat DOI
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