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缺镁大鼠异丙肾上腺素诱发心室颤动的发生率增加。

Enhanced incidence of isoproterenol-induced ventricular fibrillation in the magnesium-deficient rat.

作者信息

Guideri G, Lehr D, Horowitz S

出版信息

J Am Coll Nutr. 1985;4(2):139-55.

PMID:4019937
Abstract

The electrocardiogram was recorded and serum and bulk myocardial electrolytes were determined in male Sprague Dawley rats, subjected to dietary magnesium deficiency for various periods, to assess the time course of development and cessation of the enhanced arrhythmogenic action of isoproterenol (150 micrograms/kg, subcutaneously) and to establish possible relationships between electrolyte changes and severe ventricular dysrhythmias. Ventricular fibrillation occurred within 60 min following isoproterenol injection in 25, 25, 62.5, 50, and 62.5% of rats on magnesium deficient diet for 4, 7, 11, 15, and 19 days (N = 8), respectively, and resulted in death in most animals (83%). Reintroduction of normal chow following a 30-day period on magnesium-deficient diet normalized serum magnesium (from 1.42 +/- 0.23 to 1.90 +/- 0.08 mEq/liter, mean +/- SD) but did not significantly reduce the incidence of ventricular fibrillation. Magnesium deficiency did not produce statistically significant alterations in bulk myocardial content of sodium, potassium, magnesium, and calcium. However, sodium was elevated and potassium diminished in hearts from rats that died in ventricular fibrillation, but not in those that had recovered. Magnesium-deficient rats sacrificed 30 min after isoproterenol injection, that is before the occurrence of ventricular fibrillation, exhibited hypomagnesemia and hypokalemia as well as elevated sodium and diminished potassium and magnesium in the myocardium. In contrast, rats on Purina Chow exhibited hypermagnesemia, but also showed hypokalemia and diminished cardiac potassium. The results indicate that magnesium deficiency enhances the arrhythmogenic propensity of isoproterenol and that the development of ventricular fibrillation is preceded by serum and myocardial electrolyte alterations.

摘要

对雄性斯普拉格-道利大鼠进行不同时期的饮食性镁缺乏处理,记录其心电图并测定血清和心肌总体电解质,以评估异丙肾上腺素(150微克/千克,皮下注射)增强致心律失常作用的发生和停止的时间进程,并确定电解质变化与严重室性心律失常之间可能的关系。在饮食性镁缺乏4、7、11、15和19天的大鼠(每组8只)中,分别有25%、25%、62.5%、50%和62.5%在注射异丙肾上腺素后60分钟内发生心室颤动,且大多数动物(83%)因此死亡。在缺镁饮食30天后重新给予正常饲料,可使血清镁恢复正常(从1.42±0.23毫当量/升升至1.90±0.08毫当量/升,平均值±标准差),但并未显著降低心室颤动的发生率。镁缺乏并未使心肌总体钠、钾、镁和钙含量产生具有统计学意义的改变。然而,死于心室颤动的大鼠心脏中钠升高而钾降低,但恢复的大鼠心脏中则无此现象。在注射异丙肾上腺素后30分钟处死的缺镁大鼠,即在心室颤动发生之前,表现为低镁血症和低钾血症,同时心肌中钠升高、钾和镁降低。相比之下,食用普瑞纳饲料的大鼠表现为高镁血症,但也有低钾血症和心脏钾含量降低。结果表明,镁缺乏增强了异丙肾上腺素的致心律失常倾向,且心室颤动的发生之前存在血清和心肌电解质改变。

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