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热休克蛋白90在门脉高压大鼠内脏高动力循环中的作用
作者姓名:Ai JH  Yang Z  Qiu FZ
作者单位:1. 上海第二军医大学东方肝胆外科医院生物信号传导实验室
2. 430030,武汉,华中科技大学同济医学院附属同济医院普外科
基金项目:国家自然科学基金资助项目 ( 3 0 170 92 0 )
摘    要:目的研究热休克蛋白90(HSP90)在门脉高压大鼠内脏高动力循环中的作用。方法20只SD大鼠制成门脉高压动物模型,10只大鼠行假手术作为对照。4周后处死动物获取肠系膜动脉。测定其对甲氧胺(MTX)和乙酰胆碱的量效曲线。然后再灌注格尔德霉素(GA),再次测量其量效曲线。去内膜后,再测量肠系膜动脉对硝普钠(SNP)的量效曲线。结果肠系膜动脉对MTX的反应性降低。而GA能增强门脉高压大鼠肠系膜血管对MTX的反应性。GA还能减少肠系膜血管乙酰胆碱依赖的血管扩张,但不能减少SNP依赖的血管扩张。结论本研究说明了HSP90在门脉高压大鼠内脏高动力循环中起重要作用。

关 键 词:热休克蛋白90  门脉高压症  大鼠  内脏高动力循环  动物模型  甲氧胺  乙酰胆碱

Role of heat shock protein 90 in hyperdynamic circulation of portal hypertensive rats
Ai JH,Yang Z,Qiu FZ.Role of heat shock protein 90 in hyperdynamic circulation of portal hypertensive rats[J].National Medical Journal of China,2004,84(1):9-13.
Authors:Ai Jian-hua  Yang Zhen  Qiu Fa-zu
Institution:Department of Surgery, Tongji Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan 430030, China.
Abstract:OBJECTIVE: To study the role of heat shock protein 90 (HSP 90) in the formation of hyperdynamic circulation of portal hypertensive rats. METHODS: Animal model of portal hypertension was established by partial ligation of the portal vein among 20 SD rats (group P). Ten rats underwent sham operation (group S) Four weeks after the operation, the rats were killed and their mesenteric arteries and portal veins were obtained. The expression of HSP 90 in the portal veins and part of the superior mesenteric arteries was detected by Western blotting. Another mesenteric arteries underwent continuous perfusion with methoxamine (MTX, 30 and 100 micro mol/L) or acetylcholine (Ach). The perfusion pressure was monitored by a sensor. The concentration-response curves were examined in response to MTX and Ach infusion respectively. Then geldanamycin (GA) was infused; responses to MTX and ACh were repeated as described above. The endothelia of these arteries was denuded. After endothelial denudation was achieved, response to sodium nitroprusside (SNP) was examined. RESULTS: The expression of HSP 90 was much stronger in the group P than in the group S. The perfusion pressure of the mesenteric artery of the group P was 13.32 mm Hg +/- 0.55 mm Hg, significantly lower than that of the group S (17.33 mm Hg +/- 0.57 mm Hg, n = 10, P < 0.001). After the addition of MTX, the perfusion pressure of the mesenteric artery of the group P was 141.9 mm Hg +/- 7.6 mm Hg, significantly lower than that of the group S (181.1 mm Hg +/- 16.2 mm Hg, n = 8, P < 0.001). GA and 30 micro mol/L or 100 micro mol/L MTX were added successively into the perfusion fluid for the mesenteric superior artery of the group P, then the perfusion pressure became 106.7 mm Hg +/- 7.5 mm Hg or 124.9 mm Hg +/- 5.5 mm Hg, significantly higher than those of the mesenteric superior artery of the group P without addition of GA (60.9 mm Hg +/- 4.3 mm Hg, n = 5, P < 0.05 and 98.7 mm Hg +/- 4.7 mm Hg, n = 5, P < 0.05). GA and 100 micro mol/L MTX were added successively into the perfusion fluid for the mesenteric superior artery of the group S, the perfusion pressure became 151.2 mm Hg +/- 7.1 mm Hg, not significantly different from that of the mesenteric superior artery of the group S without addition of GA (149.8 mm Hg +/- 5.6 mm Hg, P > 0.05). With the addition of GA in advance, the ACh-dependent vasorelaxation of the isolated perfused rat mesenteric artery was significantly attenuated in comparison with the mesenteric artery without addition of GA into whose perfusion fluid (P < 0.05). However, GA did not affect the vasodilation of the ensothelium-neduded mesenteric artery in response to SNP. CONCLUSION: HSP90 is responsible for the hyperdynamic circulation in the portal hypertensive rats.
Keywords:Portal hypertension  Geldanamycin  Heat shock protein 90
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