摘要
目的观察大鼠急性耐力训练运动后血管收缩及舒张功能的变化并探讨其机制。方法健康雄性SD大鼠在运动平板上进行跑步适应性训练2周后，进行一周耐力训练。训练方式为平板跑，运动5d／周，耐力训练时平均运动距离2000-2300m／d。同年龄安静饲养动物为对照。运动结束时取降主动脉在体外检测血管对80mmol／L高钾溶液与1μmol／L苯肾上腺素的收缩反应，以及血管对乙酰胆碱的舒张反应。阻断-氧化氮合酶（NOS）及血红素加氧酶1（HO-1）后再次观察血管对乙酰胆碱的舒张反应。部分主动脉环进行免疫组织化学检测血管内皮HO-1。同年龄静止饲养大鼠作为对照。结果大鼠经1周耐力运动训练后，主动脉对高钾溶液的收缩反应未见明显变化，对苯肾上腺素引起的收缩反应显著减弱，对乙酰胆碱的舒张反应显著增强（P〈0．01）。NOS阻断剂预孵后，正常不运动对照大鼠血管内皮依赖性舒张被阻断达（97．7±3．3）％，经过耐力训练的大鼠血管被阻断（78．8±2．1）％（与对照组比较，P〈0．01），耐力训练组尚存的内皮依赖性舒张可被HO-1阻断剂proto—porphyrin IX Zinc（Ⅱ）进一步阻断。免疫组化结果显示主动脉血管HO-1显著增加。结论急性耐力运动训练后血管内皮依赖性舒张功能增强，该作用可能与运动诱导的血管内皮中HO-1增加有关。
Objective To observe vessel function in rats after endurance training and the possible role of heme oxygenase-1 （HO-1）. Methods Male Sprague-Dawley rats underwent endurance exercise on treadmill for 1 week （2000--2300 m/d） after a 2-week acclimation training. Rats were trained to run 5 days per week during the total course of training. Contraction responses of isolated aortic to high potassium chloride （80 mmol/L） and phenylephrine were assessed after training. Aortic relaxation to acetylcholine with and without blockade of nitric oxide synthase （NOS） and HO-1 were tested. Sedentary rats of the matched age were used as control. Aortic HO-1 were also examined with immunohistochemistry. Results Aortic contractile response to high potassium was not altered but response to s-receptor agonist was attenuated significantly in exercise trained rats as compared with controls （P〈0.01）. Endurance training improved endothelium-dependent vasodilatation （P〈0.01）. In sedentary control aorta, NOS inhibition abrogated 97.7% ± 3.3% of endothelium-dependent relaxation, which was only partially abrogated by NOS inhibition in trained rat＇s aorta（78.8% ±2.1%, P〈0.01 versus control）. The remaining relaxation to acetylcholine was further eliminated by HO-1 inhibitor protoporphyrin IX Zinc （ Ⅱ ）. Immunohistochemistry demonstrated elevation of HO-1 in aorta from endurance trained rats. Conclusion Acute endurance training enhances endothelium-dependent vasodilatation. Up-regulation of vessel HO-1 may be con- tributed partly to the enhanced vessel relaxation.
出处
《中华高血压杂志》
CAS
CSCD
北大核心
2007年第11期904-907,共4页
Chinese Journal of Hypertension
基金
国家自然科学基金重点项目(No770848)
上海交通大学基础医学院大学生自然科学研究基金(NoJTYXY05001)
