促甲状腺素释放素增敏失血性休克大鼠心脏肾上腺素受体及其机理  

Myocardial adrenoceptors sensitized by thyrotropin releasing hormone and its mechanisms during hemorrhagic shock in rats

作　　者：刘良明[1] 陈惠孙[1] 胡德耀[1] 卢儒权[1] 李金鸣[1] 张克义[1] 郝丽英[1] 王玉萍[1] 

机构地区：[1]第三军医大学野战外科研究所,中国医科大学药理学教研室

出　　处：《中国药理学与毒理学杂志》1995年第3期212-215,共4页Chinese Journal of Pharmacology and Toxicology

摘　　要：采用失血性休克大鼠离体心脏观察了促甲状腺素释放素（ＴＲＨ）对肾上腺素受体激动剂正性肌力作用的影响及对肾上腺素受体数量和亲和力的影响，并用全细胞记录式膜片钳技术研究了ＴＲＨ对豚鼠单一心肌细胞慢钙内流及其对肾上腺素受体激动剂促钙内流作用的影响。结果表明，ＴＲＨ可上调失血性休克大鼠β肾上腺素和多巴胺受体数量，并增加β肾上腺素受体的亲和力。ＴＲＨ可延长心肌细胞膜钙通道开放时间，增加异丙肾上腺素和多巴胶的促钙内流作用，ＴＲＨ的这一作用可能是其增敏心脏肾上腺素受体，增强其激动剂正性肌力作用的重要原因。The effects of thyrotropin releasinghoimone(TRH)on positive inotropic actions ofadrenergic agonists and on mvocardial adrenoceptorswere observed during hemorrhagic shock in rats;meanwhile, effects of TRH alone and combined withadrenergic agonists on calcium current in singlecardiac cell were also investigated.The resuIts indi-cated that TRH potentiated the positive inotropic ac-tions of isoprenaline and dopamine on isolated leftatrium of rat subjected to hemorrhagic shock,but itdid not potentiate the effect of phenylephrine,TRH(5 mg·kg-1)up-regulated the number of myocardialβ-adrenoceptors and dopamine receptors duringhemorrhagic shock,and increased the affinity ofβ-adrenoceptors.TRH prolonged the open durationof calcium channel and augmented the calcium ionicinward induced by isoprenaline and dopamine. It wassuggested that TRH could promote the cardiacadrenoceptors sensitivity of shocked animals.Theeffects of TRH to up-regulate myocardialadrenoceptors of shocked animal to prolongate theopen duration of calcium channel,and to increase cal-cium ionic inward of isoprenaline and dopaminemight be the mechanisms by which β-adrenoceptorsand dopamine receptors were sensitized.

关 键 词：促甲状腺释放素 TRH 休克 受体 肾上腺素能 

分 类 号：R966[医药卫生—药理学] R972[医药卫生—药学]