肽6A对家兔动脉的血管再通作用  

THE RECANALIZATION ACTION OF PEPTIDE 6 A IN RABBIT ARTERY

作　　者：张灵芝[1] 樊贵[2] 艾南南 苏静怡[1] 汤健[1] 唐朝枢[1] 沈金焕[3] 杜雨苍[3] 

机构地区：[1]北京医科大学心肺内分泌研究室 [2]张家口医学院 [3]中国科学院上海生物化学研究所

出　　处：《北京医科大学学报》1992年第2期109-111,共3页Journal of Peking University(Health Sciences)

摘　　要：在部分结扎家兔腹主动脉和电刺激造成的血栓模型上,经动脉注射肽6 A(10 μinol/kg体重),发现肚6A可明显缩小血栓,并部分恢复腹主动脉血流量和股动脉血压。本实验还观察到,血栓部位动脉管壁血管紧张素Ⅱ(AGTII)含量较非血栓部位增加91％,而肽6A治疗明显抑制该部位AGTII含量的增加。结果表明,肽6A是有效的血管再通剂,其作用机理之一可能是抑制 AGTII的合成。In this work thrombosis was produced in rabbit abdominal aorta by partial ligation and electricalstimulation of the artery. In the control group thrombus weight was 31±5 mg (n=6), in the experi-mental group (n=6) Peptide 6A (P 6 A) was administered into the cephalic end of aorta. thethrombus was significantly smaller (18±2 mg, P<0.05), and blood flow in the abdominal aorta andfemoral arterial blood pressure returned to 50±6％ and 48±3％ of the original levels (in the controlare 19±3％ and 22+2％ respectively, in both cases P<0.01). Results showed that P6 A is aneffective thrombolyzer and consequently a vascular recanalyzer. With rad oimmunoassay it is shownthat in the site of thrombus formation the arterial wall contained 91％ more angiotensin II(AGT II)than in the nonthrombotic site (P<0.01). P 6 A administration significantly inhibited the increase ofAGTII, only 19％ more than that in the nonthrombotic site. It suggested that inhibition of localsynthesis of AGTII is probably one of the chief mechanisms of the vascular recanalization action ofP 6 A.

关 键 词：血栓形成 血管紧张素Ⅱ 肽6A 

分 类 号：R965[医药卫生—药理学]