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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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001-es BibID:	BIBFORM040599
Első szerző:	Nieminen, Markku S.
Cím:	Effects of Levosimendan on the Energy Balance : Preclinical and Clinical Evidence / Markku S. Nieminen, Piero Pollesello, Gusztáv Vajda, Zoltán Papp
Dátum:	2009
Megjegyzések:	Levosimendan is a novel inodilator agent, which enhances myocardial performance without substantial changes in oxygen consumption. The combination of positive inotropic and vasodilator effects of levosimendan relates to its Ca-sensitizing and K channel opening effects. Levosimendan is one of the best documented pharmacological agents used in the management of acute heart failure syndromes. Interest in levosimendan has recently been renewed owing to its potential in supporting cardiac function in patients with ischemic heart disease and cardiogenic or septic shock. It has been also demonstrated that levosimendan can be used as a bridge therapy for the perioperative phase of cardiac surgery. The ability of levosimendan to improve myocardial function without substantially increasing oxygen consumption may appear paradoxical but is indeed possible via improved efficacy, not only with regard to the effects on the contractile apparatus of the cardiomyocytes but also when its composite hemodynamic effects are considered. The energy balance equation, therefore, should take into account the effect of levosimendan on all energy-consuming and energy-producing paths. Moreover, levosimendan-evoked KATP channel opening may possess favorable effects on mitochondrial adenosine triphosphate synthesis conferring cardioprotection during ischemic insults.
Tárgyszavak:	Orvostudományok Klinikai orvostudományok idegen nyelvű folyóiratközlemény külföldi lapban
Megjelenés:	Journal of Cardiovascular Pharmacology and Therapeutics. - 53 : 4 (2009), p. 302-310. -
További szerzők:	Pollesello, Piero Vajda Gusztáv (1956-) (kardiológus) Papp Zoltán (1965-) (kardiológus, élettanász)
Pályázati támogatás:	K 68363 OTKA
Internet cím:	Intézményi repozitóriumban (DEA) tárolt változat DOI
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