Abstract

Hypomagnesemia is a common clinical finding in hospitalized patients and can cause hypocalcemia, cardiac arrhythmias, muscular weakness, and hypokalemia. Hypomagnesemia usually implies cellular magnesium (Mg) depletion, but stress and some clinical conditions which raise serum catecholamine concentrations may lower serum Mg (sMg) concentrations. To help investigate the mechanism and degree of the effect of catecholamines on sMg concentration, we gave intravenous epinephrine (0.1 microgram/kg/min) to 12 normal volunteers for 2 hours. The sMg concentration fell from 1.86 +/- 0.04 mg/dl to 1.63 +/- 0.05 mg/dl (mean +/- SEM, p less than 0.01). Pre-infusion intracellular free Mg (Mg++) in red blood cells (RBC) as measured by nuclear magnetic resonance spectrophotometry (NMR) was 171 +/- 7.6 microM and did not differ significantly from post-infusion RBC Mg++, 186 +/- 12.6 microM. Total blood mononuclear cell Mg content and urine Mg excretion also did not change. These data suggest that epinephrine has a small but significant effect on the lowering of sMg concentrations. Endogenous catecholamine release during stress or acute illness may therefore contribute to the hypomagnesemia seen in acutely ill patients. Our data also suggest that hypomagnesemia seen under conditions of acute stress may not always imply depleted tissue Mg stores. As no absolute change in cellular Mg or in urinary Mg excretion was demonstrated, acute intracellular shifts of Mg into blood cells and/or urinary Mg losses may not account for the hypomagnesemia. The prevalence and clinical consequences of stress hypomagnesemia require further investigation.