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背景盐是心血管疾病的重要危险因素之一,其作用机制可能与氧化应激和内皮功能失调有关。目的观察慢性高盐负荷对自发性高血压大鼠(SHR)血压、氧化应激水平及内皮功能的影响。方法5周龄雄性SHR48只,高盐组(4%NaCl)、正常摄盐组(0.4%NaCl)各24只,分别饲养4、8、12、16周处死(每次每组6只),取血清测定亚硝酸盐(NOx)、丙二醛(MDA)含量及超氧化物歧化酶(SOD)活性;取胸主动脉采用免疫组织化学方法观察内皮型一氧化氮合酶(eNOS)的改变。结果在实验各阶段,高盐组的收缩压显著高于正常摄盐组[4周(158.0±13.6)比(145.0±10.9)、8周(175.0±18.5)比(149.0±8.1)、12周(178.0±14.8)比(161.0±15.3)、16周(178.0±17.1)比(159.0±17.1)mmHg,P<0.05];高盐组的NOx(P<0.01)、MDA水平(P<0.05),以及eNOS表达水平(P<0.01)均高于正常摄盐组,且随着年龄时间呈明显上升趋势;两组血清SOD水平未发现明显差异(P>0.05)。结论高盐摄入可导致体内氧化应激水平升高和内皮功能失调,这可能是其增加心血管病发病风险的机制之一。
Background Salt is one of the important risk factors of cardiovascular diseases. Its mechanism may be related to oxidative stress and endothelial dysfunction. Objective To observe the effects of chronic high salt stress on blood pressure, oxidative stress and endothelial function in spontaneously hypertensive rats (SHR). Methods Forty five male SHR48, 5% saline, 4% NaCl and 0.4% NaCl were sacrificed at 4, 8, 12 and 16 weeks (6 rats in each group) The content of nitrite (NO), malondialdehyde (MDA) and the activity of superoxide dismutase (SOD) in serum were determined by the method of immunohistochemistry. The changes of endothelial nitric oxide synthase (eNOS) . Results The systolic blood pressure of the high salt group was significantly higher than that of the normal saline group during the experimental period (158.0 ± 13.6 vs 145.0 ± 10.9, 175.0 ± 18.5, 149.0 ± 8.1, 12 weeks, (178.0 ± 14.8) vs (161.0 ± 15.3), 16 weeks (178.0 ± 17.1) vs (159.0 ± 17.1) mmHg, P <0.05] , And eNOS expression levels (all P <0.01) were higher than those of the normal saline group, and increased with age. There was no significant difference in serum SOD levels between the two groups (P> 0.05). Conclusion High salt intake may lead to the increase of oxidative stress and endothelial dysfunction in vivo, which may be one of the mechanisms of its increased risk of cardiovascular disease.