The aim of our study is detection of the possible correlation between the degree of inflammation, fibrosis of the liver and the level plasma concentration of metoprolol in the treatment of chronic heart disease. Terminal stages of liver fibrosis characterized by marked reduction of effector T cell function and activity of cells with the potential suppressor (CD4+CD25+), and B-lymphocytes and NK-cells (CD16+SD56+), which play the main role in a cascade of liver damage. In the prolonged ischemia, metabolism of metoprolol is slows and its concentration in the blood is gradually increasing, which subsequently may lead to a enhanced pharmacological effects of metoprolol and more significant blocking of β-receptors.

rTNFalpha-induced programmed death of Jurkat tumor cells cultured with 17-AAG, a selective inhibitor of heat shock protein (Hsp90), was studied by fluorescent microscopy with the use of FITC-labeled annexin V and propidium iodide. Caspase-3 and -8 activities were determined by spectrophotometry using a caspase- 3 and -8 colorimetric assay kit. It was shown that inhibition of Hsp90 leads to activation of Jurkat cell apoptosis while Hsp90 itself suppresses this process. 17-AAG enhances rTNFa-induced apoptosis of tumor cells.