Hypomagnesemia is one of the most frequent serum electrolyte abnormalities in current clinical practice. Routine inclusion of serum Mg analysis in the electrolyte panel will enhance the clinical recognition and treatment of hypomagnesemic Mg-depleted patients. Failure to respond to treatment of recurrent ventricular tachycardia/fibrillation to usual antiarrhythmic therapy in patients with acute myocardial infarction, idiopathic dilated cardiomyopathy, and congestive heart failure should alert the clinician to consider administering intravenous Mg. Repair of coexisting hypomagnesemia in hypokalemic patients is essential to avoid the problem of refractory K repletion caused by coexisting Mg depletion. More controlled clinical studies of Mg deficiency are necessary to ascertain the cost-effectiveness of Mg replacement therapy.
Studies of experimental magnesium depletion have been reported in the past (1)(2)(3)(4)(5)(6)(7)(8). This report describes a re-evaluation of this problem in which some of the previous observations have been confirmed and extended. In particular these studies were concerned with the interrelationships between magnesium deficiency and the metabolism of potassium, calcium, and phosphorus. In addition, the pathologic alterations of the kidneys were examined. These latter observations will be alluded to here, although they have been reported in an abstract (9), and will be the subject of a more detailed discussion in another publication.
METHODS A-ND EXPERINIENTAL D)ESIGNFemiale Sprague-Dawley rats were used throughout. The animals were pair-fed by groups a synthetic diet free of sodium, potassium, chloride, phosphate, and magnesium. The composition of this diet is listed in Table I. In additon, each animal received daily by gavage an approp)riate electrolyte solution which will be described in specific terms later. Demineralized water was allowed at will.At the end of each experiment the animals were anesthetized with hexobarbital sodium administered intraperitoneally, and then exsanguinated from the abdominal aorta. Thigh, leg, and lumbar muscles were taken for chemical analysis, and the other tissues obtained for histologic examination. In some experiments total carcass was also analyzed. The preparation of erythrocytes for analysis involved an initial centrifugation in a plastic tube, followed by the removal of plasma and buffy coat. The red cell mass was then recentrifuged at 20,000 g for 15 minutes. At the end of this time the tube was frozen, and then a cut was made just below the top of the erythrocyte mass. In this fashion a quantity of relatively pure red cells was obtained.The chemical methods were as follows: urea nitrogen vith the autoanalyze.r utilizing the calorimetric reaction with diacetyl monoxime (10); sodium and potassium,
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