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1.

001-es BibID:BIBFORM016143
Első szerző:Babick, Andrea P.
Cím:Sarcolemmal Remodeling in Heart Failure Due to Myocardial Infarction / Andrea Babick, Judit Barta, Naranjan S. Dhalla
Dátum:2005
Megjegyzések:Moderate degree of congestive heart failure (CHF) upon occluding coronary artery has been shown to be associated with a depression in the sarcolemmal (SL) Na+-K+ ATPase activity, as well as differential changes in mRNA levels and protein contents for different SL Na+-K+ ATPase isozymes. Likewise, the decreased SL Na+-Ca2+ exchanger activity was accompanied by depressed gene expression and protein content. Although the number of SL Ca2+-channels in the failing heart was decreased, no change in SL Ca2+-pump activity was evident. Such observations indicate that the SL membrane becomes remodeled during the development of CHF due to myocardial infarction.
Tárgyszavak:Orvostudományok Elméleti orvostudományok előadáskivonat
Megjelenés:Advances in Heart Disease : Proceedings of the 12th World Congress on Heart Disease ? New Trends in Research, Diagnosis and Treatment / ed. Asher Kimchi. - p. 3-10
További szerzők:Barta Judit (1975-) (kardiológus) Dhalla, Naranjan S.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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2.

001-es BibID:BIBFORM015749
Első szerző:Barta Judit (kardiológus)
Cím:Myofibrillar Remodeling During the Development of Ischemic Heart Disease / Barta Judit, Raja B. Singh, Srilekha Maddika, Rajat Sethi, Naranjan S. Dhalla
Dátum:2008
Megjegyzések:Ischemic heart disease (IHD) resulting from insufficient supply of O2 and nutrients is one of the major causes of moitality and morbidity in the developed as well as developing countries. Extensive studies on IHD haverevealed alterations at the cellular, subcellular and molecular levels in the ischemic cardiac muscle. It is generally believed that both the occurrences of oxidativestress and the development of intracellular calcium (Ca2+) overload are important mechanisms of cardiac dysfunction and injury to myocardium in the IHD. Myofibrílar proteins, which form an essential part of contractile machinery ofthe heart and determine the cardiac contractile activity have been shown to exhibit changes in their assembly as well as activities under a wide variety of conditions associated with IHD. The present article is aimed to provide an insight into the assembly of myofibrilar proteins and alterations in their biochemical activities to emphasize the significance of myofibrillar remodeling(changes in structure and function) in hearts subjected to ischemia as well as reperfusion. It is proposed that myofibrillar remodeling plays an important role in cardiac dysftrnction in IHD.
Tárgyszavak:Orvostudományok Elméleti orvostudományok könyvfejezet
Ischemic heart disease
myofibrillar remodeling
ischemia-reperfusion injury
Megjelenés:Recent Advances in Cardiovascular Sciences / ed. S.S. Agrawal. - p. 42-62
További szerzők:Singh, Raja B. Maddika, Srilekha Sethi, Rajat Dhalla, Naranjan S.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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3.

001-es BibID:BIBFORM015748
Első szerző:Barta Judit (kardiológus)
Cím:Modulation of renin-angiotensin system : applications in clinical cardiology / Barta Judit, Andrea P. Babick, David P. Brasil, Naranjan S. Dhalla
Dátum:2006
Tárgyszavak:Orvostudományok Elméleti orvostudományok könyvfejezet
Megjelenés:Contemporary Perspectives on Clinical Pharmacotherapeutics / eds. K. Kohli, M. Gupta, S. Tejawani. - p. 253-267
További szerzők:Babick, Andrea P. Brasil, David P. Dhalla, Naranjan S.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
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4.

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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5.

001-es BibID:BIBFORM015747
Első szerző:Dhalla, Naranjan S.
Cím:Subcellular Remodeling as a Viable Target for the Treatment of Congestive Heart Failure / Naranjan S. Dhalla, Melissa R. Dent, Paramjit S. Tappia, Rajat Sethi, Barta Judit, Ramesh K. Goyal
Dátum:2006
Megjegyzések:It is now well known that congestive heart failure (CHF) is invariably associated with cardiac hypertrophy, and changes in the shape and size of cardiomyocytes (cardiac remodeling) are considered to explain cardiac dysfunction in CHF. However, the mechanisms responsible for the transition of cardiac hypertrophy to heart failure are poorly understood. Several lines of evidence both from various experimental models of CHF and from patients with different types of CHF have indicated that the functions of different subcellular organelles such as extracellular matrix, sarcolemma, sarcoplasmic reticulum, myofibrils, mitochondria, and nucleus are defective. Subcellular abnormalities for protein contents, gene expression, andenzyme activities in the failing heart become evident as a consequence of prolonged hormonal imbalance, metabolic derangements, and cation maldistribution. In particular, the occurrence of oxidative stress, development of intracellular Ca2+ overload, activation of proteasesand phospholipases, and alterations in cardiac gene expression result in changes in the biochemical composition, molecular structure, and function of different subcellular organelles (subcellular remodeling). Not only does subcellular remodeling appear to be intimately involved in the transition of cardiac hypertrophy to heart failure, the mismatching of the function of different subcellular organelles leads to the development of cardiac dysfunction. Although blockade of the renin-angiotensin system, sympathetic nervous system, and various other hormonal actions have been reported to produce beneficial effects on cardiac remodeling and heart dysfunction in CHF, the actions of various cardiac drugs on subcellular remodeling have not been examined extensively. Some recent studies have indicated thatboth the angiotensin-converting enzyme inhibitors and angiotensin receptor antagonists attenuate changes in sarcolemma, sarcoplasmic reticulum, and myofibril enzyme activities, protein contents, and gene expression, and partly improve cardiac function in the failing hearts. It is suggested that subcellular remodeling is an excellent target for the development of improved drug therapy for CHF. Furthermore, extensive studies should investigate theeffects of different agents individually or in combination on reverse subcellular remodeling, cardiac remodeling, and cardiac dysfunction in various experimental models of CHF.
Tárgyszavak:Orvostudományok Elméleti orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
congestive heart failure
cardiac remodeling
subcellular remodeling
cardiac drugs
cardiac hypertrophy
cardiac dysfunction
Megjelenés:Journal of Cardiovascular Pharmacology and Therapeutics. - 11 : 1 (2006), p. 31-45. -
További szerzők:Dent, Melissa R. Tappia, Paramjit S. Sethi, Rajat Barta Judit (1975-) (kardiológus) Goyal, Ramesh K.
Internet cím:Intézményi repozitóriumban (DEA) tárolt változat
DOI
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6.

001-es BibID:BIBFORM095255
Első szerző:Kovács Árpád (kardiológus)
Cím:Interventricular Differences of Signaling Pathways-Mediated Regulation of Cardiomyocyte Function in Response to High Oxidative Stress in the Post-Ischemic Failing Rat Heart / Árpád Kovács, Melissa Herwig, Heidi Budde, Simin Delalat, Detmar Kolijn, Beáta Bódi, Roua Hassoun, Melina Tangos, Saltanat Zhazykbayeva, Ágnes Balogh, Dániel Czuriga, Sophie Van Linthout, Carsten Tschöpe, Naranjan S. Dhalla, Andreas Mügge, Attila Tóth, Zoltán Papp, Judit Barta, Nazha Hamdani
Dátum:2021
ISSN:2076-3921
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
folyóiratcikk
Megjelenés:Antioxidants. - 10 : 6 (2021), p. 1-21. -
További szerzők:Herwig, Melissa Budde, Heidi Delalat, Simin Kolijn, Detmar Bódi Beáta (1989-) (molekuláris biológus) Hassoun, Roua Tangos, Melina Zhazykbayeva, Saltanat Balogh Ágnes (1984-) (kardiológus) Czuriga Dániel (1982-) (kardiológus) Linthout, Sophie Van Tschöpe, Carsten Dhalla, Naranjan S. Mügge, Andreas Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Barta Judit (1975-) (kardiológus) Hamdani, Nazha
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7.

001-es BibID:BIBFORM068537
Első szerző:Kovács Árpád (kardiológus)
Cím:Myosin heavy chain and cardiac troponin T damage is associated with impaired myofibrillar ATPase activity contributing to sarcomeric dysfunction in Ca2+-paradox rat hearts / Árpád Kovács, Judit Kalász, Enikő T. Pásztor, Attila Tóth, Zoltán Papp, Naranjan S. Dhalla, Judit Barta
Dátum:2017
ISSN:0300-8177
Megjegyzések:This study aimed to explore the potential contribution of myofibrils to contractile dysfunction in Ca2+-paradox hearts. Isolated rat hearts were perfused with Krebs?Henseleit solution (Control), followed by Ca2+-depletion, and then Ca2+-repletion after Ca2+-depletion (Ca2+-paradox) by Langendorff method. During heart perfusion left ventricular developed pressure (LVDP), end-diastolic pressure (LVEDP), rate of pressure development (+?dP/dt), and pressure decay (-dP/dt) were registered. Control LVDP (127.4???6.1 mmHg) was reduced during Ca2+-depletion (9.8???1.3 mmHg) and Ca2+-paradox (12.9???1.3 mmHg) with similar decline in +dP/dt and ?dP/dt. LVEDP was increased in both Ca2+-depletion and Ca2+-paradox. Compared to Control, myofibrillar Ca2+-stimulated ATPase activity was decreased in the Ca2+-depletion group (12.08???0.57 vs. 8.13???0.19 ?mol Pi/mg protein/h), besides unvarying Mg2+ ATPase activity, while upon Ca2+-paradox myofibrillar Ca2+-stimulated ATPase activity was decreased (12.08???0.57 vs. 8.40???0.22 ?mol Pi/mg protein/h), but Mg2+ ATPase activity was increased (3.20???0.25 vs. 7.21???0.36 ?mol Pi/mg protein/h). In force measurements of isolated cardiomyocytes at saturating [Ca2+], Ca2+-depleted cells had lower rate constant of force redevelopment (ktr,max, 3.85???0.21) and unchanged active tension, while those in Ca2+-paradox produced lower active tension (12.12???3.19 kN/m2) and ktr,max (3.21???23) than cells of Control group (25.07???3.51 and 4.61???22 kN/m2, respectively). In biochemical assays, ?-myosin heavy chain and cardiac troponin T presented progressive degradation during Ca2+-depletion and Ca2+-paradox. Our results suggest that contractile impairment in Ca2+-paradox partially resides in deranged sarcomeric function and compromised myofibrillar ATPase activity as a result of myofilament protein degradation, such as ?-myosin heavy chain and cardiac troponin T. Impaired relaxation seen in Ca2+-paradoxical hearts is apparently not related to titin, rather explained by the altered myofibrillar ATPase activity.
Tárgyszavak:Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Calcium paradox
Myofibrillar ATPase activity
Isolated cardiomyocytes
Myofilament protein degradation
Megjelenés:Molecular and Cellular Biochemistry 403 : 1-2 (2017), p. 57-68. -
További szerzők:Kalász Judit (1986-) (molekuláris biológus) Pásztorné Tóth Enikő (1966-) (laboratóriumi analitikus) Tóth Attila (1971-) (biológus) Papp Zoltán (1965-) (kardiológus, élettanász) Dhalla, Naranjan S. Barta Judit (1975-) (kardiológus)
Pályázati támogatás:GINOP-2.3.2-15-2016-00043
GINOP
K116940
OTKA
K109083
OTKA
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DOI
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8.

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.
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9.

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
Dátum:2006
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
Cardiomyopathies
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
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10.

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
Dátum:2005
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
hyperthyroidism
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.
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11.

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.
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12.

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.
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