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目的 :观察长期摄入大量葡萄糖通过抑制 11β羟化固醇脱氢酶 2型导致大鼠血压升高致肾脏滋养动脉损伤的病理学改变。方法 :4 0只雄性Wister大鼠随机分为四组 ;对照组 (10只 ) ,其它三组 (各 10只 )分别给予葡萄糖 15 .0g/kg·d ,2 5 .0 g/kg·d ,35 .0 g/kg·d(分别为葡萄糖 1组、葡萄糖 2组和葡萄糖 3组 )共 3个月。分别于1月、2月和 3月末测尾动脉血压 ,3月末对大鼠肾脏滋养动脉行光镜观察摄片。结果 :与对照组比较 ,长期摄入大量葡萄糖大鼠动脉血压水平升高 (P <0 .0 1) ;肾脏滋养动脉出现平滑肌痉挛 ,平滑肌增生 ,血管壁增厚 ,血管腔变窄。结论 :长期摄入大量葡萄糖可能通过抑制 11β羟化固醇脱氢酶 2型参与了高血压的发病过程。
OBJECTIVE: To observe the pathological changes of renal nourish artery injury induced by long-term ingestion of large amount of glucose by inhibiting the blood pressure of 11β-hydroxysteroid dehydrogenase type 2 in rats. Methods: Forty male Wister rats were randomly divided into four groups. The control group (10 mice) and the other three mice (10 mice each) were given glucose 15.0 g / kg · d and 25.0 g / kg · d , 35.0 g / kg · d (glucose group 1, glucose group 2 and glucose group 3 respectively) for 3 months. Tail arterial blood pressure was measured at the end of January, February and March, respectively. At the end of March, rat kidney nourishing artery was observed under light microscope. Results: Compared with the control group, the arterial blood pressure increased significantly (P <0.01) in long-term ingestion of glucose. The kidneys showed smooth muscle spasm, smooth muscle hyperplasia, thickening of blood vessel wall and narrowing of vascular lumen. Conclusion: Long-term intake of glucose may be involved in the pathogenesis of hypertension by inhibiting 11β-hydroxysteroid dehydrogenase type 2.