Search

Start Over Subject srdeční selhání

11. Intraventricular pressure gradients in heart failure

Creator:
Guerra, M., Brás-Silva, C., Amorim, M. J., Moura, C., Bastos, P., and Leite-Moreira, A. F.
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, srdeční selhání, heart failure, intraventricular, gradients, diastole, systole, myocardial segments, 14, and 612
Language:
English
Description:
M. Guerra ... [et al.]. and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

12. Isoforms of troponin in normal and diseased myocardium

Creator:
Michaela Adamcová and Václav Pelouch
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, troponiny, myokard, srdeční selhání, ontogeneze, troponins, myocardium, heart failure, ontogeny, isoforms of troponin, congenital heart disease, 14, and 612
Language:
English
Description:
M. Adamcová, V. Pelouch. and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

13. Mechanisms of chronic heart failure development in end-stage renal disease patients on chronic hemodialysis

Creator:
Jan Malík, Vladimír Tuka, Magdaléna Mokrejšová, Robert Holaj, and Vladimír Tesař
Type:
article, články, model:article, and TEXT
Subject:
Patologie. Klinická medicína, fyziologie, srdeční selhání, hemodialýza, human physiology, heart failure, hemodialysis, volume overload, pressure overload, 14, and 616
Language:
English
Description:
More than 50 % of end-stage renal disease (ESRD) patients treated by chronic hemodialysis die from cardiovascular diseases, including congestive heart failure (CHF). The incidence of CHF is rising in both general and ESRD population. However, the mechanisms, which lead to the development of CHF in dialyzed patients, differ considerably. First, there are several factors leading to increase of the left ventricular afterload: volume overload between dialyses, hypertension, increased arterial stiffness, anemia, vascular access flow (arteriovenous fistula) and sympathetic activation. Second, hypertension, left ventricular hypertrophy, anemia and frequently present coronary artery disease worsen myocardial oxygenation. The combination of these factors explains the high incidence of CHF in dialyzed patients and their roles are reviewed in this article., J. Malík ... [et al.]., and Obsahuje seznam literatury
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

14. Modulation of myocardial stiffness by β-adrenergic stimulation - its role in normal and failing heart

Creator:
Falcãa-Pires, I., Fontes-Sousa, A. P., Lopes-Conceiçaão, Brás-Silva, C., and Leite-Moreira, A. F.
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, srdeční selhání, heart failure, β-adrenergic stimulation, diastolic function, myocardial stiffness, 14, and 612
Language:
English
Description:
The acute effects of β-adrenergic stimulation on myocardial stiffness were evaluated. New-Ze aland white rabbits were treated with saline (control group) or do xorubicin to induce heart failure (HF) (DOXO-HF group). Effects of isoprenaline (10-10-10-5 M), a non-selective β-adrenergic agonist, were tested in papillary muscles from both groups. In the control group, the effects of isoprenaline were also evaluate d in the presence of a damaged endocardial endothelium, atenolol (β1-adrenoceptor antagonist), ICI-118551 (β2-adrenoceptor antagonist), KT-5720 (PKA inhibitor), L-NNA (NO-synthase inhibitor), or indomethacin (cyclooxygenase inhibitor). Passive length-tension relations were constructed before and after adding isoprenaline (10-5 M). In the control group, isoprenaline increased resting muscle length up to 1.017±0.006 L/Lmax. Correction of resting muscle length to its initial value resulted in a 28.5±3.1 % decrease of resting tension, indicating decreased muscle stiffness, as confirmed by the isoprenaline-induced right-downwa rd shift of the passive length- tension relation. These effects were modulated by β1- and β2-adrenoceptors and PKA. In DOXO-HF group, the effect on myocardial stiffness was significantly decreased. We conclude that β -adrenergic stimulation is a relevant mechanism of acute neurohumoral modulation of the diastolic function. Furthermore, this study clarifies the mechanisms by which myocardial stiffness is decreased., I. Falcão-Pires ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

15. Natriuretic peptides - physiology, pathophysiology and clinical use in heart failure

Creator:
Jan Krupička, Tomáš Janota, Zdislava Kasalová, and Jaromír Hradec
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, srdeční selhání, natriuretické peptidy, physiology, heart failure, natriuretic peptides, heart failure diagnosis, heart failure treatment, BNP, NT-proBNP, Optima Study, 14, and 612
Language:
English
Description:
The natriuretic peptides - atrial, brain and C-type - were discovered during the last tw enty years. Their effects on cardiovascular, renal, cerebral and other tissues through guanylyl cyclase were uncovered. Over the past decade natriuretic peptides (NPs) became a very useful tool in the management of heart failure patients. Results of many clinical trials have shown that BNP and NT-proBNP are helpful for diagnosis of heart failure. They are also independent markers of prognosis not only in heart failure patients but also in patients with other cardiovascular diseases. Recently published data document the utility of NPs in guiding treatment of heart failure patients. In this article, we focus on basic biochemical and physiological characteristics of NPs as well as on their significance in management of heart failure patients. Some limitations and pitfalls of NPs levels interpretation in diagnosing heart failure are also discussed., J. Krupička ... [et al.]., and Obsahuje seznam literatury
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

16. Nitric oxide and prostaglandins - important players in endothelin-1 induced myocardial distensibility

Creator:
Brás-Silva, C., Monteiro-Sousa, D., Duarte, A. J., Guerra, M., Fontes-Sousa, A. P., Moura, C., Areias, J. C., and Leite-Moreira. A. F.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, fyziologie, endotel, srdeční selhání, physiology, endothelium, heart failure, endothelin, diastolic properties, myocardial distensibility, 14, and 612
Language:
English
Description:
This study investigated whether endothelin (ET)-1-induced increase in myocardial distensibility is preserved in heart failure (HF) and whether it is modulated by nitric oxide (NO) and prostaglandins. New Zealand white rabbits were treated with doxorubicin (1 mg/kg, intravenously twice a week for 8 weeks, DOX-HF group) or saline (control group). Effects of ET-1 (0.1, 1, 10 nM) were tested in papillary muscles from the DOX-HF group and a control group in the presence of: i) intact endocardial endothelium (EE); ii) damaged EE; iii) NG-nitro-L-arginine (L-NNA; NO synthase inhibitor), and iv) indomethacin (INDO; cyclooxygenase inhibitor). In the presence of an intact EE, ET-1 promoted concentration-dependent positive inotropic and lusitropic effects that were maintained after damaging the EE, in the presence of L-NNA or INDO and in the DOX-HF Group. ET-1 reduced resting tension at the end of the isometric twitch (increased diastolic distensibility) by 3.2±1.3 %, 6.0±1.6 % and 8.8±2.7 % (at 0.1, 1 and 10 nM, respectively), in muscles with intact EE, effect that was completely abolished after damaging EE, in the presence of L-NNA or INDO or in the DOX-HF Group. This study demonstrated that the increase in myocardial distensibility induced by ET-1 is absent in HF and is dependent of NO and prostaglandin release., C. Brás-Silva, D. Monteiro-Sousa, A. J. Duarte, M. Guerra, A. P. Fontes-Sousa, C. Moura, J. C. Areias, A. F. Leite-Moreira., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

18. Parathyroid hormone response to vitamin D insufficiency in elderly males with chronic heart failure

Creator:
Bozic, B., Loncar, G., Prodanovic, N., Lepic, T., Radojicic, Z., Cvorovic, V., Dimkovic, S., and Popovic, V.
Format:
print
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, srdeční selhání, vitamin D, heart failure, PTH, response, vitamin D insufficiency, adiponectin, bone markers, 14, and 612
Language:
English
Description:
Secondary hyperparathyroidism (SHPT) may contribute to the systemic illness that accompanies chronic heart failure (CHF). Healthy elderly with vitamin D deficiency who did not develop hyperparathyroidism (functional hypoparathyroidism, FHPT) had lower mortality than those who di d. This study was designed to examine determinants of the PTH response in the vitamin D insufficient CHF patients. Sixty five vitamin D insufficient males with NYHA class II and III and 20 control subjects age ≥ 55 years were recruited. Echocardiography, physical performance, NT-pro-BNP, PTH, 25-hydroxyvitamin D (25(OH)D), adiponectin and bone activity surrogat e markers (OPG, RANKL, OC, β-CTx) were assessed. Increased NYHA cl ass was associated with SHPT, while physical performance was inferior compared to FHPT. SHPT was associated with lower left ventricular ejection fraction (LVEF) and flow mediated dilatation, but with higher left heart dimensions, left ventricular mass index and right ventricular systolic pressure. CHF patients with SHPT had increased NT-pro-BNP, adiponectin and bone markers, but decreased 25(OH)D compared to those with FHPT. Independent determinants for SHPT in CHF patients with vitamin D insufficiency were LVEF, adiponectin and β-CTx, irrespective of renal function and serum vitamin D levels. In conclusion, increased PTH levels, but not low vitamin D, demonstrated close relation to CHF severity., B. Bozic ... [et al.]., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

19. Ryanodine receptors, voltage-gated calcium channels and their relationship with protein kinase A in the myocardium

Creator:
Miloš Petrovič, Karel Valeš, Putnikovič, B., Djulejič, V., and Mitrovič, D. M.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, biochemie, vápník, proteinové kinázy, srdeční selhání, biochemistry, calcium, protein kinases, heart failure, ryanodine receptors, calcium channels, 14, and 612
Language:
English
Description:
We present a review about the relationship between ryanodine receptors and voltage-gated calcium channels in myocardium, and also how both of them are related to protein kinase A. Ryanodine receptors, which have three subtypes (RyR1-3), are located on the membrane of sarcoplasmic reticulum. Different subtypes of voltage-gated calcium channels interact with ryanodine receptors in skeletal and cardiac muscle tissue. The mechanism of excitation-contraction coupling is therefore different in the skeletal and cardiac muscle. However, in both tissues ryanodine receptors and voltage-gated calcium channels seem to be physically connected. FK-506 binding proteins (FKBPs) are bound to ryanodine receptors, thus allowing their concerted activity, called coupled gating. The activity of both ryanodine receptors and voltage-gated calcium channels is positively regulated by protein kinase A. These effects are, therefore, components of the mechanism of sympathetic stimulation of myocytes. The specificity of this enzyme’s targeting is achieved by using different A kinase adapting proteins. Different diseases are related to inborn or acquired changes in ryanodine receptor activity in cardiac myocytes. Mutations in the cardiac ryanodine receptor gene can cause catecholamine-provoked ventricular tachycardia. Changes in phosphorylation state of ryanodine receptors can provide a credible explanation for the development of heart failure. The restoration of their normal level of phosphorylation could explain the positive effect of beta-blockers in the treatment of this disease. In conclusion, molecular interactions of ryanodine receptors and voltage-gated calcium channels with PKA have a significant physiological role. However, their defects and alterations can result in serious disturbances., M. M. Petrovič, K. Valeš, B. Putnikovič, V. Djulejič, D. M. Mitrovič., and Obsahuje bibliografii a bibliografické odkazy
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public

20. S100A1: a major player in cardiovascular performance

Creator:
Cuarte-Costa, S., Castro-Ferreira, R., Neves, J. S., and Leite-Moreira, A. F.
Format:
print, bez média, and svazek
Type:
article, články, model:article, and TEXT
Subject:
Fyziologie člověka a srovnávací fyziologie, srdeční selhání, genová terapie, endoteliální dysfunkce, heart failure, gene therapy, endothelial dysfunction, calcium homeostasis, contractile function, 14, and 612
Language:
English
Description:
Calcium cycling is a major determinant of cardiac function. S100A1 is the most abundant member of the calcium-binding S100 protein family in myocardial tissue. S100A1 interacts with a variety of calcium regulatory proteins such as SERCA2a, ryanodine receptors, L-type calcium channels and Na+/Ca2+ exchangers, thus enhancing calcium cycling. Aside from this major function, S100A1 has an important role in energy balance, myofilament sliding, myofilament calcium sensibility, titin-actin interaction, apoptosis and cardiac remodeling. Apart from its properties regarding cardiomyocytes, S100A1 is also important in vessel relaxation and angiogenesis. S100A1 potentiates cardiac function thus increasing the cardiomyocytes’ functional reserve; this is an important feature in heart failure. In fact, S100A1 seems to normalize cardiac function after myocardial infarction. Also, S100A1 is essential in the acute response to adrenergic stimulation. Gene therapy experiments show promising results, although further studies are still needed to reach clinical practice. In this review, we aim to describe the molecular basis and regulatory function of S100A1, exploring its interactions with a myriad of target proteins. We also explore its functional effects on systolic and diastolic function as well as its acute actions. Finally, we discuss S100A1 gene therapy and its progression so far., S. Duarte-Costa, R. Castro-Ferreira, J. S. Neves, A. F. Leite-Moreira., and Obsahuje bibliografii
Rights:
http://creativecommons.org/licenses/by-nc-sa/4.0/ and policy:public