摘要
目的:观察醛固酮对正常和心衰大鼠肠系膜阻力血管的急性作用并研究其可能机制。方法:结扎SD大鼠冠状动脉左前降支,建立心衰模型;取肠系膜血管三级分支约2 mm长血管环,通过PowerLab生物信号采集系统记录张力变化。结果:醛固酮预处理10 min,随着苯肾上腺素(PE)浓度的增加,正常大鼠肠系膜阻力血管收缩率与对照组相比先降低后升高,心衰大鼠则降低,该效应可部分被醛固酮特异受体阻断剂依普利酮阻断;醛固酮可使正常和心衰大鼠乙酰胆碱诱导的内皮依赖性血管舒张反应均较对照组显著增强;醛固酮和地塞米松共孵育10 min后,醛固酮对两种肠系膜阻力血管收缩率的改变都被部分抵消,在正常大鼠上地塞米松的这种效应可被糖皮质激素受体拮抗剂RU486阻断。结论:醛固酮对正常大鼠PE诱导的肠系膜阻力血管的收缩效应具有双向作用,减弱了心衰大鼠肠系膜阻力血管对PE的敏感性;地塞米松可部分取消正常大鼠醛固酮对血管的双向作用,对心衰大鼠作用不明显。
Objective ： To investigate the acute effects of aldosterone （ALD） on mesenteric resistance vessels in normal or heart failure （HF） rats and its mechanism. Methods： HF model was adopted by in vivo ligation of left anterior descending coronary artery in SD rats; segments of third-order branches of mesenteric artery were isolated and dissected into about 2 mm rings for isometric force recording. Results： Pretreated with ALD for 10 min ,phenylephrine （PE）-induced contraction of normal mesenteric artery decreased first and then increased compared to control group along with the increase of the concentration of PE while decreased in HF rats. This effect was attenuated by ALD receptor-special antagonist eplerenone partially. ALD increased Ach-induced endothelial-dependent vascular relaxation significantly compared to control group both in normal and HF rats. Pretreated with ALD and dexamethasone （DEX） for 10 rain, the effects of ALD on PE-induced contraction were weakened in mesenteric artery both of normal and HF rats. And this reaction of DEX to ALD-treated mesenteric in normal rats was attenuated by RU486 partially. Conclusions： ALD has biphasic effect in PE-induced response on mesenteric artery of normal rats, while reduces the sensitivity of mesenteric artery to PE in HF rats. DEX attenuates the biphasic effect of ALD on artery of normal rat partially but has no significant effect on that of HF rats.
出处
《浙江大学学报（医学版）》
CAS
CSCD
北大核心
2013年第1期92-97,共6页
Journal of Zhejiang University(Medical Sciences)
关键词
心力衰竭
药物疗法
醛固酮
治疗应用
血管阻力
药物作用
肠系膜动脉
地塞米松
治疗应用
疾病模型
动物
Heart failure/drug therapy
Aldosterone/therapeutic use
Vascular resistance/drug effects
Mesenteric arteries
Dexamethasone/therapeutic use
Disease models, animal
