促甲状腺素释放激素改善失血性休克心功能的作用机理  

The cardiovascular mechanism of thyrotropin-releasing hormone in experimental hemorrhagic shock

作　　者：郑达[1] 陈惠孙[2] 胡德耀[2] 

机构地区：[1]成都军区昆明总医院全军创伤外科中心,昆明650032 [2]第三军医大学野战外科研究所,重庆630042

出　　处：《中国药理学与毒理学杂志》1990年第4期248-250,共3页Chinese Journal of Pharmacology and Toxicology

摘　　要：TRH iv后显著升高失血性休克家兔MAP,±dP/dt_(max),Vpm,V_(max)和血浆E。利血平预处理后,TRH的上述作用消失。β受体阻滞剂普萘洛尔预处理后,TRH增强±dP/dt_(max),Vpm和V_(max)的作用消失,并在iv TRH后20和30 min取消了TRH的升压作用。α受体阻滞剂酚苄明预处理后,TRH仍能升高MAP,±dP/dt_(max),Vpm和V_(max)。离体大鼠左心房实验证明TRH(0.1mmol/L)可显著增强异丙肾上腺素和多巴胺的正性肌力作用。Thyrotropin-releasinghormone(TRH)could improve mean arterial pressure(MAP)and myocardial contractile parameters(± dP/dtmax,Vpm and Vmax)and increased plasma epinephrine(at 10 min post-treatment)significantly in hemorrhagic shock.The effects of TRH on MAP and contractility disappeared in reserpinized(4 mg/kg,24 h pre-treatment,iv)rabbits.TRH had no effects on myocardial contractility and MAP(at 20 and 30 min post-treatment)in pre-treated rabbits with propra-nolol(1 mg/kg,1 h pre-treatment,iv).Nevertheless,it had effects on myocardial contractility and MAP in pre-treated rabbits with phenoxybenzamine(1mg/kg,1 h pre-treatment,iv).Experiments in vitro showed that although TRH(0.1 mmol/L)had no direct effct on the heart,left atrium and aortic strip,it could potentiate the inotropic effects of isoprenaline(0.5μg/ml)and dopamine(10μg/ml)on the left atrium.These results suggested that TRH had some relations with catecholamine to increase the myocardial contractility and MAP.It might act on sympatho medullary system to secrete epinephrine and sensitize the β-receptors,but not α-receptors.Thus,TRH improved cardiac contractility,cardiac output and hemodynamics during hemorrhagic shock.The sensitization of the β-receptors and dopamine receptors might play an important role in the direct peripheral mechanisms of TRH.

关 键 词：TRH 失血性休克 心血管功能 

分 类 号：R972.5[医药卫生—药品]