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作 者:杨万松[1] 黄体钢[1] 周丽娟[1] 樊振旺[1] 王蔚群[1]
出 处:《实用心脑肺血管病杂志》1999年第3期140-143,共4页Practical Journal of Cardiac Cerebral Pneumal and Vascular Disease
基 金:天津市科委资助研究课题
摘 要:目的 探讨转换酶抑制剂对肾性高血压大鼠血浆、主动脉内皮细胞NO和ATⅡ生成的影响。方法 雄性Wistar大鼠40只,20只结扎一侧肾动脉后分为A、B两组各10只,B组服用依那普利,另10只不结扎肾动脉作为对照组。术后三周测血压、血浆一氧化氮和血管紧张素Ⅱ,留24小时尿测尿去甲肾上腺素和肾上腺素水平。余下10只大鼠断颈处死取主动脉做内皮细胞培养,传至第四代时植入24孔板,8孔一组进行药物干预试验,分别设对照组,两种浓度的胰岛素(A_1、A_2)、卡托普利(B_1、B_2 )、去甲肾上腺素(C_1、C_2)和肾上腺素(D_1、D_2)组。培养24小时后测上清液一氧化氮和血管紧张素Ⅱ含量。结果 A组大鼠血压、血管紧张素Ⅱ和尿去甲肾上腺素较对照组和B组显著升高,一氧化氮显著降低。B组大鼠血压、血管紧张素Ⅱ较A组降低,一氧化氮较A组升高,与对照组无明显差异。不同浓度的胰岛素可使内皮细胞一氧化氮生成增加,对血管紧张素Ⅱ无明显影响。卡托普利可促进一氧化氮生成,抑制血管紧张素Ⅱ产生。高浓度的去甲肾上腺素抑制一氧化氮生成,增加血管紧张素Ⅱ产生。肾上腺素对一氧化氮生成无明显影响,却抑制血管紧张素Ⅱ生成。结论 血管紧张素转换酶抑制剂恢复肾性高血压大鼠一氧化氮含量,并减少尿儿茶酚胺排泄。而胰岛素可促进内皮细胞一氧化氮?To investigate the effects of angiotensin converting enzyme inhibitor (ACEI) on the production No and AT II in plasma and endothelium cells in rats. Methods After left renal artery uncompletely ligated,20 male Wis-tar rats were divided into A and B subgroup containing 10 rats in each, enalapril was given in subgroup B,10 others as control. Systolic blood pressure, plasma nitric oxide (NO ),angiotensin II (AT II ) and urinary noradrenaline and adrenaline levels were measured at the 3rd week after opera-tion. The 10 surplus rats were killed by. decapitation, endothlium cell (EC) of aorta were cultrured. Insulin, captopril, noradrenaline and adrenaline were uesed to test the function of EC producing NO and AT H . Results At the 3rd week, systolic blood pressure, AT II and urinary noradrenaline were increased and NO decreased in subgroup A than in B and control. In cultrured EC,insulin prompted the production of NO, had no effect on AT II , captopril increased NO and decreased AT II generation,high level of noradrenaline de- craesed NO and increased AT II generation. Conclusion ACEI may increase NO production and inhibit the excretion of urinary noradrenaline and adrenaline,and insulin may prompt the generation of NO in cultrured EC, but it has no effect on AT II .
分 类 号:R544.140.5[医药卫生—心血管疾病]
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