摘要
笔者观察了促甲状腺素释放激素(TRH)对失血性休克大鼠在体和离体组织cAMP水平的影响,结果显示大鼠失血性休克发展到一定严重程度时,心室肌、肝组织和肾皮质cAMP水平明显下降。TRH(4mg/kg BW,ⅳ)治疗可逆转这些改变,在普奈洛尔(propranolol)预处理的失血性休克大鼠,TRH的这种作用消失。离体实验中,TRH本身不影响肝组织cAMP水平,但能明显增加异丙肾上腺素刺激肝组织cAMP的产生,普奈洛尔可消除TRH的这种作用。本研究结果表明,TRH提高组织cAMP水平与增敏β受体有关,TRH通过提高组织cAMP水平调节细胞的代谢和功能,起到抗休克作用。
The investigation was designed to further elucidate the antishock mechanism of thyrotropin—releasing hormone (TRH). The effect of TRH on cyclic AMP levels in tissue of rats in hemorrhagic shock was studied. The results indicateed that the cyclic AMP levels of heart ventricle muscle, liver and renal cortex decreased significantly as shock prolonged. TRH (4mg/kg BW. iv) treatment could raise cyclic AMP levels of these tissues, but its effect was abolished by propranolol pretreatment. In vitro. the liver slices cyclic AMP response to isoprenaline (ISO) was significantly decreased in hemorrhagic shock compared to controls. TRH (10^(-6)—10^(-4)M) itself didn't alter cyclic AMP level, but increased ISO stimulating liver cyclic AMP accumulation. The level of cyclic AMP in liver slices incubated with TRH+Iso was significantly higher than that of incubated with Iso alone. This effect of TRH also was abolished in the presence of propranolol (10^(-6)M). Based on these results, it can be concluded that: (1) Hemorrhagic shock reduced the tissue response to beta adrenergic stimulating, cyclic AMP levels in tissue decreased significantly. (2) TRH treatment could raise tissue cyclic AMP levels, which is closely related to its sensitizing beta—adrenergic receptor. (3) The beneficial effect of TRH on hemorrhagic shock came true by raising tissue cyclic AMP which regulate the cell metabolism and function.
出处
《中华创伤杂志》
CAS
CSCD
北大核心
1993年第5期280-282,共3页
Chinese Journal of Trauma
