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镁缺乏条件下心肌的致心律失常阈值。

Arrhythmogenic threshold of the myocardium under conditions of magnesium deficiency.

作者信息

Spasov A A, Iezhitsa I N, Kharitonova M V, Gurova N A

机构信息

Institute of Pharmacology; Department of Pharmacology, Volgograd State Medical University, Russia.

出版信息

Bull Exp Biol Med. 2008 Jul;146(1):63-5. doi: 10.1007/s10517-008-0208-1.

DOI:10.1007/s10517-008-0208-1
PMID:19145352
Abstract

We studied the arrhythmogenic threshold of the myocardium after injection of CaCl2 to magnesium-deficient rats receiving Mg2+ L-aspartate, MgCl2, their combination with vitamin B6, and reference preparations Magne B6 and MgSO4 until complete compensation of magnesium level in the plasma and erythrocytes. Magnesium-deficient diet and deionized water were used for inducing alimentary Mg2+ deficiency and modeling pathological changes in rats. After reducing Mg2+ level to 0.7 mmol/liter in the plasma and to 1.5 mmol/liter in erythrocytes, Mg L-aspartate, MgCl2, their combination with vitamin B6, as well as Mg2+ deficiency led to a decrease in the dose of CaCl2 provoking heart rhythm disturbances in 50% animals and shortening of animal life span. Administration of the test magnesium salts increased the arrhythmogenic threshold; Mg2+ salts were comparable by their efficiency with Magne B6 and were far superior to MgSO4.

摘要

我们研究了向缺镁大鼠注射氯化钙后心肌的致心律失常阈值,这些缺镁大鼠接受了L-天冬氨酸镁、氯化镁、它们与维生素B6的组合以及参比制剂Magne B6和硫酸镁,直至血浆和红细胞中的镁水平完全得到补偿。采用缺镁饮食和去离子水诱导大鼠出现营养性镁缺乏并模拟其病理变化。在血浆中镁水平降至0.7 mmol/升、红细胞中降至1.5 mmol/升后,L-天冬氨酸镁、氯化镁、它们与维生素B6的组合以及镁缺乏均导致引发50%动物心律失常的氯化钙剂量降低,以及动物寿命缩短。给予受试镁盐可提高致心律失常阈值;镁盐的效果与Magne B6相当,且远优于硫酸镁。

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Bull Exp Biol Med. 2008 Jul;146(1):63-5. doi: 10.1007/s10517-008-0208-1.
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