Myocardial contractility and performance capacity after magnesium infusions in young healthy persons: A double‐blind, placebo‐controlled, cross‐over study

Abstract

Summary: To evaluate the effect of intravenous magnesium (Mg) treatment on the inotropic state of the heart and maximal work capacity, 9 healthy volunteers were entered in a double-blind, placebo-controlled, cross-over study. Separated by an interval of three weeks, the volunteers were tested twice, each time randomly allocated to receive either an intravenous injection of 10 mmol magnesium chloride dissolved in 100 ml isotonic sodium chloride or placebo of isotonic sodium chloride only. Before and after each infusion myocardial inotropism was evaluated by echocardiography . Mitral-septal distance (MSA) was used as a measure for ejection fraction. On each test day an ergometer bicycle exercise test was performed, and maximal work capacity was calculated. Magnesium treatment reduced the MSA (from 4.2 to 2.9 mm, p=0.07), while no difference was found after placebo treatment. Likewise, a tendency toward increasing fractional shortening after magnesium treatment was detected, although this difference was not statistically significant (p=O.l). No difference in maximal work capacity between the magnesium and placebo periods was found. Serum magnesium concentrations rose significantly after the infusions (from 0.82 to 1.38 mmol/l, p<O.OOl). It is concluded that intravenous magnesium does not exert a negative inotropic effect on the myocardium as previously stated. On the con- trary, we found a tendency toward a positive inotropic effect. However, the observed differences are of borderline statistical significance and a more extended study, employing invasive measurements of cardiac inotropism appears to be necessary.

Dialysate magnesium level and blood pressure

“…It has been systematically shown that magnesium salt infusion lowers BP via a reduction of TPR despite a moderate increase in cardiac output [8,[26][27][28]. The latter is accomplished via increases in HR and coronary flow [27] or a direct myocardial effect [28][29], independent of changes in preload, afterload, heart rate, or flow [29].…”

“…The latter is accomplished via increases in HR and coronary flow [27] or a direct myocardial effect [28][29], independent of changes in preload, afterload, heart rate, or flow [29]. These Mg-induced direct or indirect vasodilatory effects are dose dependent [27] and can be elicited at plasma concentrations as low as 1.38 mmol/L [28], while a concentration of 1.8 to 3.0 mmol/L has been suggested for treatment of eclamptic convulsions [27]. According to our data, the substantial intradialytic fall of BP seen with a HD solution containing Mg and Ca concentrations of 0.25 mmol/L and 1.25 mmol/L, respectively, was due to an unusual impairment of myocardial contractility not compensated by an increased TPR.…”

“…It has been systematically shown that magnesium salt infusion lowers BP via a reduction of TPR despite a moderate increase in cardiac output [8,[26][27][28]. The latter is accomplished via increases in HR and coronary flow [27] or a direct myocardial effect [28][29], independent of changes in preload, afterload, heart rate, or flow [29]. These Mg-induced direct or indirect vasodilatory effects are dose dependent [27] and can be elicited at plasma concentrations as low as 1.38 mmol/L [28], while a concentration of 1.8 to 3.0 mmol/L has been suggested for treatment of eclamptic convulsions [27].…”

The therapeutic use of magnesium in anesthesiology, intensive care and emergency medicine: a review

“…In a preparation of isolated animal heart, Mg, because of its anticalcium properties, caused a dose-dependent negative inotropic effect. 19 Rasmussen et al observed a moderate positive inotropic effect after infusion of Mg into healthy volunteers, 20 which could have been related to the vascular effect of Mg in reducing systemic arterial 20 and pulmonary artery pressures through a decrease of vascular resistance. 18 In in vitro studies on isolated aorta, the absence of Mg potentiated the vasoconstrictive effect of angiotensin and acetylcholine, and hypermagnesemia induced the relaxation of smooth muscle.…”

Possible pharmacological actions of magnesium in acute myocardial infarction.

“…A slight fall in blood pressure and rise in heart rate may be seen and the ratepressure product is unaltered. The haemodynamic response is similar in normal subjects and untreated hypertensives (Mroczek et al, 1977;Nadler et al, 1987;Rasmussen et al, 1988b) and in men with coronary artery disease (Borschat et al, 1988). Nadler et al (1987) infused 25 mmol MgSO4 over 3 h in normal subjects and observed a mean fall of 10 mm Hg in systolic and diastolic blood pressure, a 22% increase in renal blood flow and a 60% increase in urinary excretion of 6-keto-PGF1a, the stable metabolite of prostacyclin.…”