Your browser doesn't support javascript.
loading
Show: 20 | 50 | 100
Results 1 - 2 de 2
Filter
1.
Chinese Journal of Cardiology ; (12): 448-452, 2005.
Article in Chinese | WPRIM | ID: wpr-334684

ABSTRACT

<p><b>OBJECTIVE</b>The aim of study was to explore the effects of early beta-adrenergic blockade-metoprolol treatment on myocardial inflammatory cytokine expression and heart function in rats after acute myocardial infarction (AMI).</p><p><b>METHODS</b>The therapeutic effects of metoprolol on myocardial inflammation and heart function up to 4 weeks (according to the protocol of CCS-2) were studied by the rat model of AMI. Myocardial inflammation was examined by taking account of the number of lymphocytes infiltrated in the myocardium and analyzing the myocardial cytokine production including the pro-inflammatory cytokines: interleukin (IL)-1beta, 6 and tumor necrosis factor (TNF)-alpha and the anti-inflammatory cytokine: IL-10. Echocardiography was used to evaluate heart function.</p><p><b>RESULTS</b>The levels of TNF-alpha, IL-1beta, IL-6 and IL-10 in AMI group were markedly elevated compared to sham rats (P < 0.01) and the cytokines principally excreted by cardiac myocytes. After 4 weeks therapy, metoprolol reduced the production of TNF-alpha and IL-1beta and increased IL-10 levels (P < 0.05) in cardiac myocytes, but had no effect on the number of lymphocytes infiltrated in myocardium. Echocardiography showed that metoprolol markedly improved left heart function (P < 0.05).</p><p><b>CONCLUSION</b>Early metoprolol treatment can improve heart function and myocardial inflammatory cytokine expression after AMI. One immunopharmacologic mechanism underlying the beneficial effects of beta-adrenergic blockade may involve the attenuation of pro-inflammatory cytokines and the increase of anti-inflammatory cytokine levels in cardiac myocytes.</p>


Subject(s)
Animals , Male , Rats , Adrenergic beta-Antagonists , Therapeutic Uses , Cytokines , Genetics , Heart , Immunohistochemistry , Metoprolol , Therapeutic Uses , Myocardial Infarction , Drug Therapy , Allergy and Immunology , RNA, Messenger , Rats, Sprague-Dawley
2.
Chinese Journal of Cardiology ; (12): 526-528, 2005.
Article in Chinese | WPRIM | ID: wpr-334667

ABSTRACT

<p><b>OBJECTIVE</b>To study the significance of Th1/Th2 function imbalance in patients with post-infarction cardiac insufficiency.</p><p><b>METHODS</b>Forty-three MI (myocardial infarction) patients were divided into 2 groups one month after the onset according to the New York Heart Association (NYHA) classification system: group MI 1 (I, II) 25 patients and group MI 2 (III, IV) 18 patients. At the same time, the heart function was evaluated by two-dimensional echocardiography. Peripheral blood mononuclear cells (PBMCs) were collected from these patients. Cytokine-producing CD4 + T cells were quantified by 3-color flow cytometry after being stimulated with phorbol myristate acetate (PMA) and ionomycin. After being stimulated with PHA, the levels of IFN-gamma and IL-4 in culture supernatants were measured by ELISA.</p><p><b>RESULTS</b>The frequencies of IFN-gamma-producing T cells were found to be significantly higher in group MI 2 (16.8%) than that in group MI 1 (13.1%). There was no significant difference on the frequencies of IL-4-producing peripheral T cells between the two groups. The IFN-gamma level and the ratios of IFN-gamma/IL-4 in group MI 2 were significantly higher than those in group MI 1, while there was no significant difference in IL-4 levels between the two groups.</p><p><b>CONCLUSIONS</b>The Th-cell function was associated with heart function in post MI patients. The up-regulation of Th1 cell function was consistent with poor heart function, suggesting that Th1/Th2 cell function imbalance may participate in ventricular remodelling after MI.</p>


Subject(s)
Aged , Female , Humans , Male , Middle Aged , CD4-Positive T-Lymphocytes , Metabolism , Heart Failure , Allergy and Immunology , Interferon-gamma , Metabolism , Interleukin-4 , Metabolism , Myocardial Infarction , Allergy and Immunology , Th1 Cells , Th2 Cells
SELECTION OF CITATIONS
SEARCH DETAIL