Effects of magnesium chloride on cardiovascular hemodynamics in the neurally intact dog

H.S. Friedman et al. (1987)


To assess the cardiovascular actions of magnesium in neurally intact animals, magnesium chloride (14 mM/min) administered i.v., producing a peak arterial magnesium level between 4.7 and 7.2 mg/dl, was given to α-chloralose-anesthetized, open-chest dogs. Magnesium lowered heart rate by 36 ± 11 beats/min (P < .05), cardiac output by 0.7 ± 0.2 liters/min (P < .05), left ventricular (LV) peak dP/dt by 410 ± 96 mm Hg/sec (P < .05) and aortic and pulmonary artery pressures, but it did not change LV end-diastolic pressure, systemic resistance or pulmonary resistance. Coronary blood flow also decreased by 39 ± 11% (P < .05), myocardial oxygen consumption by 88 ± 22% (P < .05) and myocardial oxygen extraction by 53 ± 16% (P < .05). When heart rate was held constant, magnesium still decreased LV systolic pressure, LV peak dP/dt and coronary blood flow. The increase in serum magnesium was accompanied by an increase in serum calcium (by 1.4 ± 0.2 mg/dl; P < .05) and a fall in serum potassium (by 0.21 ± 0.1 mEq/dl; P < .05), but not by a change in serum sodium, myocardial electrolyte arteriovenous differences or arterial pH. Thus, at blood concentrations that are observed in humans after therapeutic dosages of magnesium, a depression of cardiac performance is observed int he anesthetized dog. Although magnesium produces a fall in coronary blood flow, this appears to be due at least in part to a decrease in myocardial oxygen requirements because myocardial oxygen extraction also decreases. Rapid changes in serum electrolytes accompany these hemodynamic effects.