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| 陈昆仑1，周光宇2，曹永孝3，李 洁3，刘 韡4，李宗芳1 热应激对大鼠肠系膜动脉内皮依赖性NO-、EDHF-介导舒张途径的损伤 |
| 论文编辑部-新丝路理论网 2011-03-31 15:22:38 作者:中华医学之家：http://www.xinxi85.com 来源: 文字大小:[大][中][小] |
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Title:
Heat stress reduced endothelium-dependent relaxations in rat mesenteric artery
- 文章编号:
- 1671-8259(2011)02-0161-04
- 作者:
- 陈昆仑1; 周光宇2; 曹永孝3; 李 洁3; 刘 韡4; 李宗芳1
- 1. 西安交通大学医学院第二附属医院干部病房普通外科，陕西西安 710004；2. 昆明医学院天然药物药理重点实验室，云南昆明 650031；
3. 西安交通大学医学院药理学系，陕西西安 710061；4. 西安交通大学医学院第二附属医院妇产科，陕西西安 710004
- Author(s):
- CHEN Kun-lun1; ZHOU Guang-yu2; CAO Yong-xiao3; LI Jie3; LIU Wei4; LI Zong-fang1
- 1. Department of General Surgery, the Second Affiliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an 710004; 2. Yunnan Pharmacological Laboratory of Natural Products, Kunming Medical College, Kunming 650031; 3. Department of Pharmacology, Medical School of Xi’an Jiaotong University, Xi’an 710061; 4. Department of Obstetrics & Gynecology, the Second Affiliated Hospital, Medical School of Xi’an Jiaotong University, Xi’an 710004, China
- 关键词:
- ; 热应激; 内皮依赖性舒张; 一氧化氮; 前列环素; 内皮源性超极化因子; 乙酰胆碱
- Keywords:
- ; heat stress; endothelium-dependent relaxation; nitric oxide (NO); prostaglandin I2 (PGI2); endothelium derived hyperpolarizing factor (EDHF); acetylcholine (ACh)
- 分类号:
- R33
- DOI:
- -
- 文献标识码:
- A
- 摘要:
- 摘要：目的 探讨热应激对大鼠肠系膜动脉内皮依赖性舒张功能降低的机制。方法 使用微血管张力描记系统，观察热应激大鼠肠系膜动脉环5-羟色胺预收缩后加入乙酰胆碱的舒张性改变，考察一氧化氮(NO)途径、内皮源性超极化因子(EDHF)途径以及前列环素(PGI2)途径在热应激后肠系膜动脉舒张功能的改变，反应特征表述为最大松弛百分率(Rmax)和产生一半最大松弛百分率时所需要乙酰胆碱浓度的负对数(pIC50)。结果 热应激大鼠肠系膜动脉Rmax和pIC50较正常大鼠肠系膜动脉降低，分别为(97±6)%、(52±8)%和8.67±0.59、7.66±1.33(P<0.01，P<0.05)。正常大鼠肠系膜动脉NO介导的舒张Rmax和pIC50分别为(53±6)%和6.89±0.93，在热应激后分别为(21±8)%(P<0.01)和4.91±0.31(P<0.01)；正常大鼠肠系膜动脉EDHF介导的舒张Rmax和pIC50分别为(35±14)%和6.30±0.56，在热应激后分别为(13±3)%(P<0.01)和5.23±1.07(P<0.01)；正常大鼠肠系膜动脉PGI2介导的舒张Rmax和pIC50分别为(8±3)%和5.69±0.37，在热应激后分别为(10±6)%(P>0.05)和5.74±0.79(P>0.05)。结论 热应激引起的动脉血管内皮依赖性舒张功能降低主要是损伤了NO-和EDHF-途径。
- Abstract:
- ABSTRACT: Objective To investigate the mechanisms of reduced endothelium-dependent relaxation in mesenteric artery in rats after heat stress. Methods With the myograph system, we examined the vessel dilatory responses by cumulative addition of acetylcholine (ACh) and pre-contraction with 5-hydroxytryptamine in heat stress rats and control rats. We studied the effects of nitric oxide (NO)-, prostacyclin I2 (PGI2)- and endothelium-derived hyperpolarizing factor (EDHF)-mediated relaxation in mesenteric artery after heat stress. The responses were characterized in terms of maximum relaxant effect (Rmax) and negative logarithm of the molar concentration that produced half maximum relaxation (pIC50). Results The Rmax and pIC50 were decreased from (97±6)% and (52±8)% in control rats to 8.67±0.59(P<0.01) and 7.66±1.33(P<0.05), respectively, in heat stress rats. In NO-mediated relaxation, the Rmax and pIC50 were (53±6)% and 6.89±0.93 in control rats, and (21±8)%(P<0.01) and 4.91±0.31 (P<0.01) in heat stress rats. In EDHF-mediated relaxation, the Rmax and pIC50 were (35±14)% and 6.30±0.56 in control rats, and (13±3)%(P<0.01) and 5.23±1.07(P<0.01) in heat stress rats. In PGI2-mediated relaxation, the Rmax and pIC50 were (8±3)% and 5.69±0.37 in control rats, and (10±6)% (P>0.05) and 5.74±0.79(P>0.05) in heat stress rats. Conclusion The decreased endothelium-dependent relaxation in mesenteric artery induced by heat stress damages NO- and EDHF-pathways.
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基金项目：陕西省国际合作项目(No.2008KW-19)
Supported by the International Cooperation Projects of Shaanxi Province (No.2008KW-19)
通讯作者：李宗芳，教授，博士生导师. E-mail: lzf2568@vip.sina.com
作者简介：陈昆仑(1985-)，男(汉族)，研究生在读. 主要研究方向：应激后身体变化与疾病.
中华医学之家：http://www.xinxi85.com
投稿信箱：zhyxzj85@163.com
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