氯化汞对家兔主动脉缩血管作用的机理研究  

Vasoconstrictive mechanism of mercuric chloride in rabbit aorta

作　　者：刘明[1] 马欣[1] 厉英倩[1] 白宇飞[1] 王红娟[1] 

机构地区：[1]西安交通大学医学院药理学教研室,陕西西安710061

出　　处：《西安交通大学学报（医学版）》2003年第4期315-317,共3页Journal of Xi’an Jiaotong University（Medical Sciences）

基　　金：陕西省自然科学基金资助项目 (No .99SM41 )

摘　　要：目的　研究氯化汞 (HgCl2 )对离体兔动脉环的作用及其机制。方法　采用离体血管张力实验法 ,观察氯化汞对离体主动脉环的作用及其作用是否依赖于血管内皮、细胞外钙和硝苯地平敏感的钙通道。结果　氯化汞 (HgCl2 ) 1～10 0 μmol·L- 1 可浓度依赖性地触发兔动脉环的收缩反应 ,酚妥拉明或去除血管内皮均不能改变此作用 ;在换用无钙营养液时仍有此作用 ,但最大收缩幅度下降了 (6 1.2± 3.3) % ;硝苯地平能呈浓度依赖性抑制HgCl2 的最大收缩反应。结论　HgCl2 引起的离体兔动脉环收缩反应主要与HgCl2 促进细胞外钙通过硝苯地平敏感的钙通道内流和细胞内钙释放有关 ,并且以细胞外钙内流为主 ;而与血管内皮和αObjective To investigate the effect of mercuric chloride (HgCl 2) on isolated aortic rings in rabbit and probe its mechanisms. Methods Isolated vascular methods were used to study the effects of HgCl 2. Results HgCl 2 (1～100?μmol·L -1) produced a concentration-dependent contractile responses of rabbit aorta. This effect could not be blocked by 100?μmol·L -1 of phentolamine or without endothelium. The maximum responses were decreased by (61.2±3.3)% in free-Ca 2+ KH solution. The contractile responses to HgCl 2 were inhibited by nifedipine in a concentration-dependent manner. Conclusion The results suggest that in vascular smooth muscles of rabbit aorta , contractile responses to HgCl 2 may be associated with influx of Ca 2+ from outside of cells through nifedipine-sensitive calcium channel and release of stored Ca 2+ , mainly with influx of Ca 2+ from outside of cells, but are not associated with α-adrenoceptor or endothelium.

关 键 词：氯化汞 家兔 主动脉 血管收缩 硝苯地平 血管内皮 毒性作用 

分 类 号：R331.3[医药卫生—人体生理学] R995[医药卫生—基础医学]