阿替洛尔对人血淋巴细胞β受体密度及血前列腺素水平的影响  

Effect of Atenolol on Human Blood Lymphocyte β-adrenoceptorDensity and Blood Prostaglandins Levels

作　　者：余细勇[1] 饶曼人[1] 林曙光 

机构地区：[1]南京医科大学,广东省心血管病研究所

出　　处：《基础医学与临床》1998年第2期64-68,共5页Basic and Clinical Medicine

基　　金：国家自然科学基金

摘　　要：本文研究１２名健康志愿者连续多次口服β阻滞剂阿替洛尔后，外周血淋巴细胞β受体密度（Ｂｍａｘ）和血浆６－酮－前列腺素Ｆ（６－ｋｅｔｏ－ＰＧＦ）／血栓素（ＴＸＢ２）的动态变化，观察β阻滞剂对正常生理状态下受体密度的调节和血浆血管活性物质的影响。结果显示，服药后第３、５、７天，Ｂｍａｘ均值较基础值分别增加４５、５６和６７％，６－ｋｅｔｏ－ＰＧＦ（较基础值有增加趋势，均值分别增加８５、１０６和６９％。这一结果提示，β阻滞剂可能具有除拮抗交感神经以外的其它有益作用。ln order to clearify if the β-adrenergic receptor and prostacyclin synthesis can be regulated directly by β-blocker , the β-adrenoceptor density in blood lymphocytes and 6-keto-prostaglandin F1u(6-keto-PGF1u)/thromboxane B2(TXB2) in plasma were investigated in 12 healthy volunteers who accepted oral administration of atenolol (AT) with multiple-dosages. The results demon- strated that the mean values of β-adrenoceptor density were increased by 45 %, 56 % and 67% re- spectively following 3- , 5- and 7-day with atenolol treatment. Although there were no significant differences in 6-keto-PGF1u/TXB2 ratio , atenolol tended to increase prostacyclin synthesis. Com- pared with basal values ,the mean values of 6-keto-PGF1u were increased by 85 %, 1 06 % and 69 % respectively at 3- , 5- and 7-day with atenolol treatment. These findings suggest that β-blocker may be of some other mechanisms in addition to antiadrenergic effect.

关 键 词：阿替洛尔 人血淋巴细胞 Β受体 前列腺素 

分 类 号：R972[医药卫生—药品]