缺血心肌β受体脱敏现象及机制探讨  

Desensitization of β-adrenoceptor During Myocardial Ischemia and Mechanism Investigation

作　　者：唐铁军[1] 吴伟康[1] 别平华[2] 卢汉平[3] 刘秀琴[3] 

机构地区：[1]中山医科大学中西医结合研究所 [2]第一军医大学微生物学教研室,广东广州510515 [3]中山医科大学放免检测中心,广东广州510089

出　　处：《中山大学学报（医学科学版）》2000年第S1期53-55,76,共4页Journal of Sun Yat-Sen University:Medical Sciences

基　　金：中国博士后基金!资助项目 ([1999] 10 );广东省中医药管理局基金!资助项目 (995 6 4)

摘　　要：【目的】观察心肌缺血状态下 β1肾上腺素能受体 (β1 AR)脱敏现象 ,探讨其脱敏的机制。【方法】用大剂量垂体后叶素 (Pit)造成大鼠心肌缺血 ,采用放射配基受体结合分析测定心肌细胞膜 β1 AR密度 ,放免测定大鼠外周血及心肌组织中cAMP水平 ,定量RT PCR方法测定β1 AR及β1 AR激酶 (βARK 1)mRNA的表达。【结果】心肌缺血时 β1 AR密度上调 ,但亲和力下降 ,血浆及心肌cAMP水平低于正常组 (P <0 0 1或P <0 0 5 ) ,βARK 1mRNA表达明显增加 (P <0 0 1)。【结论】心肌缺血时β AR数目和功能存在分离现象 ,这种现象是β AR脱敏而引起的 ,其脱敏的机制与 β ARK1mRNA表达增加有关。Objective To investigate the mechanism of desensitization of β 1-adrenoceptor(β 1-AR) during myocardial ischemia. Methods Myocardial ischemia models of rats were induced by given a booster doses of pituitrin. The density of β 1-AR on cardiac membranes was detected by radioligand binding assay. The cAMP levels of plasma and myocardium were detected by radioimmunoassay. The mRNA expression of β-AR and β-adrenoceptor kinase (β-ARK) were detected by RT-PCR assay. Results In cardiac membranes of ischemic myocardium the density of β-AR were increased but the affinity were decreased. The cAMP levels in plasma and myocardium of myocardial ischemia group were lower than control group(P<0 01 or P<0 05). The mRNA expression of β ARK-1 were significantly increased in the ischemic group. Conclusion There is a division tendency between the amount and function of β 1-AR during myocardial ischemia. It is caused by the desensitization of β 1-AR. The mechanism of desensitization is due to the increasing of mRNA expression of β ARK-1.

关 键 词：心肌缺血 受体 肾上腺素能β1 脱敏 β1肾上腺素能受体激酶 

分 类 号：R363[医药卫生—病理学]