血凝酶对大鼠离体胸主动脉环收缩作用的影响

Effect of reptilase on the contraction of rat thoracic aorta circle in vitro

目的:研究血凝酶(Reptilase,RTA)对离体大鼠胸主动脉的收缩作用与机制。方法:制备离体大鼠胸主动脉环,经生物信号采集与分析系统测定血管环的张力变化。分有内皮组和去内皮组,采用累计加药法,观察血凝酶对去氧肾上腺素(PE)和氯化钾(KCl)预收缩的胸主动脉环收缩张力的影响。结果:血凝酶对PE预收缩的胸主动脉环产生浓度依赖性的收缩作用,对内皮完整PE预收缩血管环组显著高于去内皮组;而对KCl预收缩的胸主动脉环张力无显著影响;在内皮完整的血管,预孵内皮素转化酶抑制剂磷阿米酮(phosphoramidone,5×10-6mmol/L,PAMD)后,血凝酶对PE预收缩张力明显低于未孵育组(P<0.01);在去内皮的血管环上,应用EDTA(3mmol/L)螯合细胞外Ca2+或LaCl3(100μmol/L)后,可明显阻断血凝酶对PE预收缩作用(P<0.01)。结论:血凝酶对PE预收缩的胸主动脉环的收缩作用呈浓度依赖性,其机制可能为有内皮细胞途径参与,促进内皮素释放,对PE缩血管产生协同效应;还可能与血管平滑肌上有受体操纵性钙通道(receptor-operated calcium chan-nel,ROCC)[1]参与,增加血管平滑肌钙内流有关。

Objective ： To explore the effect of reptilase （ RTA ） on the contraction and mechanism of thoracic aorta isolated from rats. Methods ： After preparation of the rat thoracic aorta tings, the tension of the tings was measured by biological signal analytical system. The two groups of endothelium-denuded aorta tings and endothelium-intact aorta tings were undergone cumulative dose increase of the drug for observing effects of reptilase on the contraction of isolated rat thoracic aorta circle pretreated by phenylephrine （ PE ） and potassium chloride （ KC1 ） , respectively. Results： Reptilase resulted in concentration-dependent contraction of the aorta tings pre-constricted by PE. The contraction induced by PE was much stronger in the group of endothelium-intaet than in endothelimn-denuded aorta rings, but no significant difference was found for the contraction induced by KCl in the two groups. On observation of the vessels with intact endothelium undergone pre-ineubation of endothelin converting en- zyme inhibitor phosphoramidone （ PAMD, 5 × 10^-6 mmol/L） , reptilase showed weaker enhancement to PE-indueed contraction as compared with that free of incubation （ P 〈 0.01 ）. The endothelium-denuded vascular rings,after chelating extraeellular Ca^2＋ or LaC13 by EDTA, markedly inhibited the enhancement of reptilase to PE-indueed contraction. Conclusion： Reptilase may cause concentration-dependent contraction of aorta tings pre-constricted with PE. The mechanism may be attributable to involvement of endothelial cells to provoke the release of endothelin through vascular constriction induced by PE. Still, It may also be involved in the receptor-operated calcium channel in the vascular smooth muscle, which can promote the calcium influx of vascular smooth muscle.