Literature DB >> 10806830

[Regulation of myocardium beta-adrenoceptors pathway in ventricular remodeling of heart failure patients].

H Jiang1, G Dai, Z Feng.   

Abstract

To study the role of myocardium beta-adrenoceptors pathway in ventricular remodeling of heart failure patients. beta-adrenegic receptor density (Bmax) and the content of cAMP were measured in the papillae of left ventricle and blood lymphocyte of 20 patients suffered from heart failure (CHF) (NYHZ classification II to III) Bmax were investigated using 3H-dihydroalpheolol as ligand. cAMP were assessed by competitive immunoassay. Left ventricle mass index (LVMI) were measured using echocardiogram. The results showed that the Bmax and cAMP in failing myocardium significantly negatively correlated with LVMI (r = -0.77, P < 0.01 and r = -0.46 P < 0.05 respectively); the Bmax of myocardium and blood lymphocyte in CHF patients with NYHA III (63 +/- 12 fmol/mgpro and 514 +/- 115 fmol/10(7) cell) significantly lowered than that of NYHA II patients (94 +/- 20 fmol/mgpro and 702 +/- 138 fmol/10(7) cell); and the Bmax of myocardium and blood lymphocyte in patients with abnormal LVMI (62 +/- 12 fmol/mgpro and 516 +/- 122 fmol/10(7) cell) decreased more significantly than that with normal LVMI patients; even in nromal LVMI patients (92 +/- 21 fmol/mgpro and 682 +/- 146 fmol/10(7) cell), the Bmax of blood lymphocyte was already decreased (P < 0.01), when comparing with controls. The intralymphocyte cAMP content sygnificantly decreased than that of controls (P < 0.05). These results indicated that Bmax could reflect the severity of ventricle remodeling and the impairment of myocardium. The regulation of myocardium intracellular messenger transduction was earlier than the pathologic structural change of LV remodeling.

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Year:  1998        PMID: 10806830     DOI: 10.1007/bf02888472

Source DB:  PubMed          Journal:  J Tongji Med Univ        ISSN: 0257-716X


  10 in total

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Journal:  Cardiovasc Res       Date:  1992-06       Impact factor: 10.787

  10 in total

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