Model of cardiovascular injury in magnesium deficiency
Model of cardiovascular injury in magnesium deficiency
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DOI：
10.1054/mehy.2000.1123
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发表时间：
2001-01-01
影响因子：
4.7
通讯作者：
Shivakumar, K
中科院分区：
文献类型：
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作者：
Shivakumar, K
已知镁缺乏会引起心血管病变。然而，目前尚不清楚是什么构成镁缺乏症-降低血清水平，降低组织水平或降低细胞内水平的离子形式的元素。本文引用证据支持一种假设，即血清镁水平的下降可能引发一系列事件，包括血管收缩、血流动力学改变和血管内皮损伤，产生促炎、促氧化和促纤维化作用，导致初始血管周围心肌纤维化，进而导致心肌损伤和替代纤维化。此外，血管紧张素II可能是镁缺乏症的致病级联反应的原动力。重要的是，这种心血管损伤的机制将独立于心肌或血管组织镁水平的降低。(C)2001年哈考特出版社有限公司
Magnesium deficiency is known to produce cardiovascular lesions. It is, however, not clear as to what constitutes magnesium deficiency - reduced serum levels, reduced tissue levels or reduced intracellular levels of the ionic form of the element. This article cites evidence in support of a hypothesis that a fall in serum magnesium levels may trigger a temporal sequence of events involving vasoconstriction, hemodynamic alterations and vascular endothelial injury to produce pro-inflammatory, pro-oxidant and pro-fibrogenic effects, resulting in initial perivascular myocardial fibrosis which, in turn, would cause myocardial damage and replacement fibrosis. Further, angiotensin II may be the prime mover of the pathogenetic cascade in magnesium deficiency. Importantly, such a mechanism of cardiovascular injury would be independent of a reduction in myocardial or vascular tissue levels of magnesium. (C) 2001 Harcourt Publishers Ltd.