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一氧化氮和一氧化氮合酶在冷应激性高血压形成中的变化
引用本文:石红梅,何丽华,张颖,叶康平,唱斗,刘童童,王生. 一氧化氮和一氧化氮合酶在冷应激性高血压形成中的变化[J]. 中华劳动卫生职业病杂志, 2007, 25(4): 197-199
作者姓名:石红梅  何丽华  张颖  叶康平  唱斗  刘童童  王生
作者单位:100083,北京大学公共卫生学院劳动卫生与环境卫生学系
摘    要:目的研究一氧化氮(NO)及一氧化氮合酶(NOS)在冷应激性高血压(CIH)中的变化情况。方法60只雄性SD大鼠适应性饲养2周后随机分为正常对照组(25±1)℃和寒冷暴露组(4±1)℃,每天暴露4 h,持续6周,每周测量2次大鼠的血压和心率。每组又分为3个小组,分别在暴露第2、4、6周处死,观察其血浆超氧化物歧化酶(SOD)、丙二醛(MDA)、心肌匀浆NO和NOS水平的变化。结果(1)暴露组大鼠血压从第2周开始明显升高[(94.16±3.81)mm Hg],与对照组[(88.77±4.45) mm Hg]比较,差异有统计学意义(P<0.01);随着暴露时间的延长,血压继续升高,至第6周达到最高,暴露组[(116.78±3.79)mm ng]与对照组[(86.19±2.79)mm Hg]的差异有统计学意义(P<0.01);而对照组大鼠血压在整个实验过程中变化不明显。(2)随着血压升高,大鼠血浆SOD活力下降,从第2周持续到第6周,与相应的对照组比较,差异有统计学意义(P<0.05);血浆MDA的水平有所升高,但与对照组相比,差异无统计学意义(P>0.05);心肌NOS活力从第2周开始降低,至第4周与对照组的差异有统计学意义(P<0.01),持续到第6周;心肌NO含量有所降低,但与对照组的差异无统计学意义(P>0.05)。结论寒冷暴露能诱发大鼠CIH模型,随着血压升高,氧化应激水平增强,而NO含量和NOS活力降低,提示NO、NOS参与了CIH的形成。

关 键 词:寒冷  高血压  一氧化氮  一氧化氮合酶  氧化性应激
修稿时间:2006-10-08

Changes of nitric oxide and nitric-oxide synthase in the development of cold-induced hypertension
SHI Hong-mei,HE Li-hua,ZHANG Ying,YE Kang-ping,CHANG Dou,LIU Tong-tong,WANG Sheng. Changes of nitric oxide and nitric-oxide synthase in the development of cold-induced hypertension[J]. Chinese journal of industrial hygiene and occupational diseases, 2007, 25(4): 197-199
Authors:SHI Hong-mei  HE Li-hua  ZHANG Ying  YE Kang-ping  CHANG Dou  LIU Tong-tong  WANG Sheng
Affiliation:Department of Occupational and Environmental Health, School of Public Health, Peking University, Beijing 100083, China
Abstract:OBJECTIVE: To study the changes of nitric oxide(NO) and nitric-oxide synthase(NOS) in the development of cold-induced hypertension (CIH). METHODS: Sixty male Sprague-Dawley adult rats were used. Thirty were exposed to cold (4 +/- 1) degrees C as cold-treated group while the other 30 were at (25 +/- 1) degrees C as controls, 4 hours a day for 6 weeks for both groups. Systolic blood pressure (SBP) and heart rate were measured twice every week. Each group was further subdivided into three groups, 10 rats each. A subgroup of the cold-treated and control rats were sacrificed at 2, 4 and 6 week. Plasma was saved to measure superoxide dismutase (SOD) and malondiadehycle (MDA), while heart was homogenated to measure NO, NOS. RESULTS: 1 SBP increased during 6 weeks of exposure to cold. From the second week, SBP of cold-treated group [(94.16 +/- 3.81) mm Hg] was significantly greater than that of control group [(88.77 +/- 4.45 mm Hg), P<0.01]. The highest SBP level was achieved at the sixth week [(116.78 +/- 3.79)mm Hg, P<0.01]. 2 Compared to the control group, SOD in cold-treated group decreased significantly from the second week, and maintained throughout the time of exposure to cold (P<0.05). MDA levels did not differ significantly between cold-treated and control groups though it increased mildly during 6 weeks of cold exposure (P>0.05). Heart NOS in cold-treated group decreased significantly from the fourth week to the sixth week. And a mild decrease was observed in heart NO of cold-treated group during 6 weeks of exposure (P>0.05). CONCLUSION: Cold-induced hypertension is induced in rats after repeated exposure to cold. The levels of NOS, NO decrease accordingly to the rise of blood pressure. This indicates that the dysfunction of NO and NOS is involved in the development of CIH.
Keywords:Chills  Hypertensien  Nitric oxide  Nitric-oxide synthase  Oxidative stress
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