CCL

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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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2.

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
Borító:
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