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1.
Bull Exp Biol Med ; 158(5): 614-6, 2015 Mar.
Artigo em Inglês | MEDLINE | ID: mdl-25778645

RESUMO

The levels of IL-8 and IL-10 and their ratio depending on the stage and NYHA functional class of heart failure were determined in the patients with chronic heart failure in comparison with healthy individuals. The level of IL-8 and IL-8/IL-10 ratio in patients were significantly higher than in controls, and the level of IL-10, significantly lower. The comparison of cytokine levels in patients at different stages of heart failure and NYHA class revealed no significant differences. However, the level of IL-10 tended to decrease by stage 3 of the disease. Significantly elevated IL-8 level along with reduced IL-10 level and significantly increased IL-8/IL-10 ratio indicated predominance of proinflammatory activity in patients with chronic heart failure, which along with the tendency to decrease IL-10 level at stage 3 of the disease may indicate the ineffectiveness of compensatory mechanisms and progressive "failure" of compensation with increasing severity of the disease.


Assuntos
Doença Crônica , Insuficiência Cardíaca/metabolismo , Idoso , Feminino , Humanos , Interleucina-6/metabolismo , Interleucina-8/metabolismo , Masculino , Pessoa de Meia-Idade
2.
Ter Arkh ; 86(9): 119-23, 2014.
Artigo em Russo | MEDLINE | ID: mdl-25518517

RESUMO

Chronic heart failure (CHF) is a serious health problem today. Despite all advances in modern medicine, the high morbidity and mortality rates of CHF force physicians to search for new more effective methods for its control. At the same time, the fact that the designing of new effective medicaments is complex and expensive and that patients show low compliance with drug therapy increases the value of non-drug treatments for heart failure, such as patient education, higher treatment compliance, which make it possible to significantly enhance the efficiency of current combined drug therapy, to improve quality of life, and, possibly, to reduce future heart failure death rates.


Assuntos
Fármacos Cardiovasculares/uso terapêutico , Insuficiência Cardíaca , Qualidade de Vida , Doença Crônica , Quimioterapia Combinada/métodos , Quimioterapia Combinada/psicologia , Insuficiência Cardíaca/tratamento farmacológico , Insuficiência Cardíaca/fisiopatologia , Insuficiência Cardíaca/psicologia , Humanos , Adesão à Medicação , Educação de Pacientes como Assunto
3.
Horm Metab Res ; 41(10): 778-84, 2009 Oct.
Artigo em Inglês | MEDLINE | ID: mdl-19544245

RESUMO

Neuroendocrine factors play an important role in the pathogenesis of chronic heart failure. Despite numerous clinical and experimental studies, the role of the hypothalamic-pituitary-adrenal axis and glucocorticoid hormones is not fully characterised. Here we present a study of plasma cortisol concentration in 74 chronic heart failure patients, divided into four groups based on NYHA functional classes I-IV, and in 17 control subjects. In parallel, we performed morphological analysis of the hypothalamic-pituitary-adrenal axis components from 8 male patients who had died from chronic heart failure, and 9 male controls. In our study we applied immunohistochemical method and quantitative analysis to investigate an expression of hypothalamic neurohormones (corticotropin-releasing hormone, vasopressin) and adrenocorticotropin hormone in the pituitary, as well as performed general histological examination of the adrenal cortex. Measurement of morning cortisol concentration in plasma of chronic heart failure patients revealed neither difference compared to controls nor with the severity of the disease. Despite this, a two-fold increase in the density of corticotropin-releasing hormone-immunoreactive neurons as well as a two-fold increase in the number of corticotropin-releasing hormone neurons co-expressing vasopressin in the hypothalamic paraventricular nucleus were found. In the anterior pituitary the density of adrenocorticotropin hormone-immunoreactive cells was significantly increased. General histological analysis of the adrenal cortex revealed a drastic thinning of the zona fasciculata and dystrophic changes in corticocytes. Structural changes, observed in the adrenal cortex, suggest a relative glucocorticoid deficiency, which may contribute to corticotropin-releasing hormone and adrenocorticotropin hormone upregulation in hypothalamus and pituitary of chronic heart failure patients.


Assuntos
Insuficiência Cardíaca/metabolismo , Hidrocortisona/sangue , Sistema Hipotálamo-Hipofisário/metabolismo , Sistema Hipófise-Suprarrenal/metabolismo , Hormônio Adrenocorticotrópico/análise , Adulto , Idoso , Idoso de 80 Anos ou mais , Hormônio Liberador da Corticotropina/análise , Feminino , Humanos , Imuno-Histoquímica , Masculino , Pessoa de Meia-Idade , Vasopressinas/análise
4.
Usp Fiziol Nauk ; 34(3): 3-20, 2003.
Artigo em Russo | MEDLINE | ID: mdl-12942758

RESUMO

Chronic heart failure (CHF) is a common complication of patients with heart dysfunction and of those suffering from various chronic illnesses. Although recently developed therapies revolutionized treatment of CHF, life expectancy of the survivors is still significantly reduced. Proposed neurohoromonal approach in CHF treatment is on the whole rather unsatisfactory. Recently the interest of clinical investigators has been focused on immune mechanisms in the pathogenesis of CHF. In this review we tried to summarize data concerning contribution of inflammatory cytokines to pathogenesis of CHF. The source and site of action of pro- and antiinflammatory cytokines and number of interactions among cytokines and neuroendocrine systems under CHF are considered. Finally we discuss novel therapies managing correction of both immune and neurohormonal status of the patient.


Assuntos
Insuficiência Cardíaca/etiologia , Neuroimunomodulação , Sistemas Neurossecretores/fisiopatologia , Animais , Fator Natriurético Atrial/fisiologia , Quimiocinas/fisiologia , Doença Crônica , Citocinas/fisiologia , Insuficiência Cardíaca/imunologia , Insuficiência Cardíaca/terapia , Humanos , Interleucina-1/fisiologia , Interleucina-10/fisiologia , Interleucina-6/fisiologia , Sistema Renina-Angiotensina/fisiologia , Sistema Nervoso Simpático/fisiopatologia , Fator de Necrose Tumoral alfa/fisiologia
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