摘要
每只大鼠iv人工合成的心房肽Ⅲ(APⅢ)5μg ,5min后,可使麻醉大鼠左室收缩压(LVSP),+LV dJP/dt_(max),每搏指数(SVI),心指数(CI),平均劝脉压(MBP)分别自用药前的18.9±s0.9,756±56,532±28,202±11,13.2±0.4降至16.6±0.7kPa,587±50 kPa·s^(-1),481±18 μ1·beat^(-1)·kg^(-1),178±6 ml·min^(-1)·kg^(-1),11.7±0.5 kPa,心率(HR).总外周阻力指数(TPRI)则无明显变化,用6-羟多巴胺去交感神经末梢后,APⅢ的上述抑制效应明显减弱.APⅢ1～100 nmol·L^(-1)不影响电刺激驱劝的豚鼠离体左心房基础收缩力,也不抑制不应期电场刺激诱发的正性变力效应,以上结果提示,APⅢ的心脏泵功能抑制效应可能依赖于交感神经系统的完整性,与心交感神经末梢去甲肾上腺素的释放无关。
Intravenous injection of synthetic atriopeptin Ⅲ (AP Ⅲ, 5μg) to the anesthetized rats produced a significant reduction in mean blood pressure in association with the inhibition of cardiac functions. Mean blood pressure, left ventricular pressure, stroke volume index, cardiac index and +LV dP / dtmax were decreased from (x± s), 13.2± 0.4,18.9 ?0.9, 532± 28, 202± 11, 756± 56 to 11.7± 0.5 kPa, 16.6± 0.7 kPa, 481± 18 μ1·bear-1·kg-1, 178± 6 ml·min-1·kg-1 and 587± 50 kPa·s-1, respectively. The heart rate and total peripheral resistance index remained unchanged. Chemical sympathectomy by 6-hydro-xydopamine markedly attenuated the hypotensive and cardiac suppressive effects of APⅢ. AP Ⅲ at concentrations of 1-100 nmol·L-1 inhibited neither basal contractility of the isolated guinea pig myocardium paced by square pulse nor positive inotropic effect induced by refractory electric field stimulation. It was proposed that the cardiac depressant effects of AP Ⅲ depended on the completion of sympathetic nervous system and had no relation with norepinephrine release from cardiac sympathetic terminals.
出处
《中国药理学与毒理学杂志》
CAS
CSCD
北大核心
1992年第1期41-43,共3页
Chinese Journal of Pharmacology and Toxicology
关键词
心房肽
血压
心输出量
心脏
atriopeptin in blood pressure cardiac output sympathetic nervous system6-hydroxydopamine heart
