Adrian Marcus, Chanut Evelyne, Laurant Pascal, Gaume Vincent, Berthelot Alain
EA3921 Metabolic and cellular optimisation, Université de Franche-Comté, UFR Sciences Médicales et Pharmaceutiques, Besançon, France.
J Hypertens. 2008 Jan;26(1):44-52. doi: 10.1097/HJH.0b013e3282f09f68.
The present study aimed to show whether long-term moderate magnesium (Mg)-deficient (150 mg/kg) and Mg-supplemented (3200 mg/kg) diets (versus control diet: 800 mg/kg), modified the occurrence of cardiovascular risk induced by aging in the rat.
Cardiovascular and arterial functions were determined by a systemic hemodynamic study and by ex vivo measurements of vasoconstriction and endothelium dependent-vasorelaxation. Arterial wall structure was determined using pressure myograph chamber and histomorphometric methods.
The main changes observed in old rats (96 weeks old) fed a control diet, in comparison to adult rats (16 weeks old) were increased pulse pressure, a loss of aortic endothelium-dependent relaxation, increased aortic wall thickness and a decrease of the aortic wall elastin/collagen ratio. Long-term moderate Mg deficiency progressively increased systolic blood pressure. Intra-arterial pulse pressure was higher in Mg-deficient old rats than in age-matched control rats. Histological examination showed that Mg deficiency increased the age-induced deleterious effects on composition and structure of aorta (media thickness, increased collagen content and reduction in the elastin/collagen ratio), which lead to large artery rigidity. Hypertension and increased pulse pressure may have contributed to the increase in the mortality rate observed in the hypertensive Mg-deficient group. Although the long-term Mg-supplemented diet lowered blood pressure and decreased the mortality rate, it had no significant effect on aortic wall thickening and stiffening.
It is suggested that a long-term and moderate Mg-deficient diet increases age-induced arterial thickness and stiffness in rats, and thus increases the cardiovascular risks incurred by aging.
本研究旨在表明长期适度缺镁（150毫克/千克）和补镁（3200毫克/千克）饮食（与对照饮食：800毫克/千克相比）是否会改变大鼠衰老诱导的心血管风险的发生情况。
通过全身血流动力学研究以及血管收缩和内皮依赖性血管舒张的体外测量来确定心血管和动脉功能。使用压力肌动描记室和组织形态计量学方法确定动脉壁结构。
与成年大鼠（16周龄）相比，喂食对照饮食的老年大鼠（96周龄）观察到的主要变化包括脉压增加、主动脉内皮依赖性舒张功能丧失、主动脉壁厚度增加以及主动脉壁弹性蛋白/胶原蛋白比率降低。长期适度缺镁会逐渐增加收缩压。缺镁老年大鼠的动脉内脉压高于年龄匹配的对照大鼠。组织学检查表明，缺镁会增加衰老对主动脉成分和结构产生的有害影响（中膜厚度增加、胶原蛋白含量增加以及弹性蛋白/胶原蛋白比率降低），从而导致大动脉僵硬。高血压和脉压增加可能导致了缺镁高血压组观察到的死亡率上升。虽然长期补镁饮食可降低血压并降低死亡率，但对主动脉壁增厚和僵硬没有显著影响。
提示长期适度缺镁饮食会增加大鼠衰老诱导的动脉厚度和僵硬程度，并因此增加衰老带来的心血管风险。
