摘要
在麻醉大鼠研究静注胍基丁胺(AGM)对血流动力学的影响,并初步探讨其机制。结果如下:(1)静注AGM(10mg/kg)后,HR,MAP,LVP,±LVdp/dtmax,CI和TPRI均明显下降;(2)预先静注NOS抑制剂LNNA(15mg/kg)或腹腔内注射鸟苷酸环化酶抑制剂亚甲基蓝(50mg/kg),均不能阻断AGM的降压作用;(3)预先静注咪唑啉受体和α2肾上腺素能受体阻断剂idazoxan(2mg/kg)则可明显阻抑AGM的降压效应。以上结果表明,AGM对麻醉大鼠的降压机制,在于显著抑制心肌收缩性而使心输出量降低,以及舒张外周血管致使总外周阻力下降;此效应似主要由IR和/或α2AR所介导。
The hemodynamic effects of intravenous injection of agmatine and their cellular mechanism were investigated in anesthetized rats. The results obtained are as follows. (1) Following intravenous injection of agmatine (10 mg/kg), HR, MAP, LVP, LV dp/dtmax, CI and TPRI were significantly decreased. (2) Pretreatment with NnitroLarginine (15 mg/kg) or methylene blue (50 mg/kg), did not affect the hypotensive effect of agmatine. (3) The hemodynamic effects induced by agmatine could be inhibited by prior intravenous injection of idazoxan (2 mg/kg), an 2adrenoceptor (2AR) and imidazoline receptor antagonist. The results indicate that the hypotensive effect induced by iv agmatine may be attributed to the decrease in cardiac output resulting from depression of myocardial contractility, as well as to the reduction in total peripheral resistance resulting from vasodilatation. These effects of agmatine may be mediated by imidazoline receptor and/or 2AR.
出处
《生理学报》
CAS
CSCD
北大核心
1999年第2期229-233,共5页
Acta Physiologica Sinica