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首页> 外文期刊>The Journal of toxicological sciences >Dysfunction of blood pressure regulation in hyperhomocyteinemia model in rats
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Dysfunction of blood pressure regulation in hyperhomocyteinemia model in rats

机译:大鼠高血红蛋白血症模型的血压调节功能障碍

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摘要

Hyperhomocysteinemia (HHC) has been reported to be one of risk factors for cardiovascular disease. We investigated the effects of HHC on blood pressure regulation and its association with damage to the thoracic aorta and imbalance of redox in plasma in rats. Rats were fed a methionine enriched diet (Met diet) or a methionine and cholesterol (Met+Chol diet) enriched diet for 16 weeks to create a subchronic HHC model, in which the plasma concentration of homocysteine was about 7 times higher than that of control rats. The increase in systolic blood pressure (Δ-SBP) from sympathetic stimulation by L-epinephrine was 2- to 3-fold larger in HHC model in rats than that in control rats after several weeks of the treatment. These findings suggest that HHC deteriorates vaso-regulatory function, which could bring on an increased risk of cardiovascular events in humans. In addition, some of the elastic lamellae in the aorta were disrupted in the HHC group. However, the content of cross-linkages which give elasticity and mechanical strength in the lamellae, was not significantly different between HHC and control rats. Also plasma concentrations of thiobarbituric acid reactive substance and glutathione as indicators for redox balance in plasma were not different. In conclusion, the deterioration of vaso-regulation in HHC model in rats might be caused by the damage to elastic lamellae in the aorta, and not by oxidative stresses.
机译:高同型半胱氨酸血症(HHC)是心血管疾病的危险因素之一。我们调查了HHC对血压调节的影响及其与大鼠主动脉损伤和血浆中氧化还原失衡的关系。给大鼠喂食富含蛋氨酸的饮食(Met饮食)或富含蛋氨酸和胆固醇(Met + Chol饮食)的饮食持续16周,以创建亚慢性HHC模型,其中高半胱氨酸的血浆浓度比对照组高约7倍。大鼠。在治疗数周后,HHC模型大鼠的L-肾上腺素交感刺激引起的收缩压(Δ-SBP)升高是对照组的2至3倍。这些发现表明,HHC破坏了血管调节功能,从而可能增加人类发生心血管事件的风险。此外,HHC组的主动脉中的一些弹性薄片被破坏了。但是,HHC和对照组大鼠之间产生弹性和机械强度的交联含量没有显着差异。同样,血浆中硫代巴比妥酸反应性物质和谷胱甘肽的浓度作为血浆中氧化还原平衡的指标也没有差异。总之,大鼠HHC模型中血管调节的恶化可能是由于主动脉中弹性片的损伤引起的,而不是由于氧化应激引起的。

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