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地高辛与心血管疾病中的膜钠钾ATP酶抑制作用

Digoxin and membrane sodium potassium ATPase inhibition in cardiovascular disease.

作者信息

Ravi Kumar A, Kurup P A

机构信息

Department of Medicine, Medical College Hospital, Thiruvananthapuram.

出版信息

Indian Heart J. 2000 May-Jun;52(3):315-8.

PMID:10976153
Abstract

Kerala has a high incidence of mucoid angiopathy, metabolic syndrome X and endomyocardial fibrosis. Magnesium deficiency has been reported in these disorders even though the Keralite diet has adequate magnesium. A possible cause of magnesium deficiency is the increased digoxin, a potent inhibitor membrane Na(+)-K+ ATPase which can lead to magnesium depletion. Digoxin is known to be synthesised by the hypothalamus and other tissues and can also be obtained from plant sources in the diet. Inhibition of Na(+)-K+ ATPase can cause intracellular magnesium depletion and increase in intracellular calcium. In view of these, a study has been carried out on the activity of membrane Na(+)-K+ ATPase, using RBC membrane, serum digoxin, magnesium and glycosaminoglycan levels in patients of mucoid angiopathy, endomyocardial fibrosis and syndrome X. Significant decrease in the membrane Na(+)-K+ ATPase was observed in patients while serum digoxin levels showed an increase. Serum magnesium was significantly lower while glycosaminoglycan levels were increased. The inhibition of Na(+)-K+ ATPase activity may be due to increase in endogenous and/or exogenous digoxin. This inhibition leads to depletion of intracellular magnesium and an increase in intracellular calcium load. The role of underlying magnesium-related insulin resistance and the consequence of this intracellular magnesium and calcium alteration in the pathogenesis of these disorders is discussed.

摘要

喀拉拉邦黏液样血管病、代谢综合征X和心内膜心肌纤维化的发病率很高。尽管喀拉拉邦人的饮食中有足够的镁,但在这些疾病中仍有镁缺乏的报道。镁缺乏的一个可能原因是地高辛增加,地高辛是一种有效的膜钠钾ATP酶抑制剂,可导致镁耗竭。已知地高辛由下丘脑和其他组织合成,也可从饮食中的植物来源获得。钠钾ATP酶的抑制可导致细胞内镁耗竭和细胞内钙增加。鉴于此,利用黏液样血管病、心内膜心肌纤维化和综合征X患者的红细胞膜、血清地高辛、镁和糖胺聚糖水平,对膜钠钾ATP酶的活性进行了一项研究。患者的膜钠钾ATP酶显著降低,而血清地高辛水平升高。血清镁显著降低,而糖胺聚糖水平升高。钠钾ATP酶活性的抑制可能是由于内源性和/或外源性地高辛增加。这种抑制导致细胞内镁耗竭和细胞内钙负荷增加。本文讨论了潜在的镁相关胰岛素抵抗的作用以及这种细胞内镁和钙改变在这些疾病发病机制中的后果。

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