Low extracellular magnesium results in cardiac failure in isolated perfused rat hearts.

Previous studies on isolated blood vessels indicate that acute withdrawal of extracellular magnesium ions ([Mg2+]o) induces calcium-dependent contractile responses, including coronary blood vessels. The present study, using isolated perfused rat hearts, was designed to assess whether low [Mg2+]o could result in cardiac failure and to gain some insight into the mechanism of action. The results show that both the myocardial oxygen consumption (by 29-38%) and oxygen tension in the coronary effluent decreased (by 18-26%) as the [Mg2+]o was decreased stepwise from 1.2 to 0.6, 0.3 and 0.0 mM. Linear-regression analysis of a plot of coronary flow versus the rate of oxygen consumption shows that there is a tendency for a rightward shift of this relationship in low [Mg2+]o and a leftward shift of the curve in elevated [Mg2+]o (4.8 mM). The experiments also show that with low [Mg2+]o, coronary flow declines 20-37%, and cardiac output and stroke volume fall 24-50% accompanied by 3- to 4-fold elevations in lactate production and eventual, irreversible cardiac failure. An interesting finding, of this study, is that the alpha-adrenoceptor constrictor agonist, phenylephrine (1-5 microM), was found to have effects very similar to low [Mg2+]o. This latter finding is consonant with our hypothesis that progressive lowering of extracellular, ionized magnesium initiates progressive coronary vasoconstriction, decreased tissue oxygenation and myocardial ischemia, which given time, in situ, in the intact host can lead to cardiac failure.