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At least 919 records · Page 51Linked to original sources
PubMed2002

Magnesium deficiency during lactation as a precipitant of ventricular tachyarrhythmias.

A young ICD recipient with a history of syncope and idiopathic polymorphic ventricular tachycardia/ventricular fibrillation presented after an ICD discharge. She had delivered her first child 8 days prior to the event and she had been lactating. Numerous short runs of polymorphic ventricular tachycardia/ventricular fibrillation resolved with aggressive replacement of magnesium and elimination of breast-feeding.

Adult↗
PubMed1978

Alcohol withdrawal and magnesium deficiency in mice.

DBA/2J mice exposed to chronic alcohol (ethanol) intoxication were found to have lower whole brain magnesium (Mg) concentrations than control animals. The symptoms of alcohol withdrawal were found to be strikingly similar to those seen in Mg deficient mice exposed to a low Mg diet without alcohol exposure. These findings suggest that CNS Mg deficits produced by alcohol exposure could contribute to the observed alcohol withdrawal syndrome. Serum Mg concentrations were also determined, and low correlations (less than or equal to 0.3) were found with brain Mg concentrations.

Alcoholism↗
PubMed1987

Glucose homeostasis in magnesium-deficient rats.

Glucose homeostasis was studied in rats fed diets containing 750,200, or 100 mg/kg Mg for 6 to 8 weeks, from the age of 4 weeks. Weight gain of the rats receiving 200 and 100 mg/kg diets was decreased. This resulted from both a lower food intake and reduced effectiveness of the ingested food. Fed or fasting plasma glucose levels were similar in the three groups. During an intravenous glucose tolerance test, the rate of glucose disappearance was higher in Mg 100 rats than in controls. By contrast, during an oral glucose tolerance test, the rise in plasma glucose was greater and more sustained in Mg 100 rats. During both tests, the insulin response was markedly lower in Mg-deficient rats than in controls. This could be partially due to the reduced insulin content of the pancreas of these animals. The impairment of tolerance to oral glucose was corrected by 5 weeks on a high-Mg diet. After intravenous injection of insulin, the fall in plasma glucose levels was also slightly more pronounced in Mg 100 rats. During no test did we observe a significant difference between glucose or insulin responses in Mg 200 or Mg 750 rats. These results, thus, show that chronic Mg deficiency alters several parameters of glucose homeostasis in the rat.

Animals↗
PubMed1994

Magnesium homeostasis and clinical disorders of magnesium deficiency.

OBJECTIVE: To survey the causes of clinical hypomagnesemia and Mg deficiency. The relationship of hypomagnesemia to digitalis toxicity, congestive heart failure, arrhythmias, and acute myocardial infarction is discussed, as is the clinical interrelationship of Mg and K concentrations, the principal intracellular cations. DATA SOURCES: A MEDLINE search and retrieval was used to identify relevant references. STUDY SELECTION: Clinical reports, as well as studies, were selected for this review. DATA EXTRACTION: There were very few placebo-controlled clinical studies. Clinical observations were related primarily to compilation of series in which Mg was administered and clinical results reported. In addition, conclusions derived from review articles on the subject of clinical Mg depletion were used. DATA SYNTHESIS: Clinical diagnosis of Mg deficiency is ascertained most expeditiously by estimating serum Mg concentrations. Although available on order by physicians, the lack of routine serum Mg analysis as part of the "electrolyte panel" impedes the diagnosis of clinical Mg deficiency. Renal loss of Mg resulting from the widespread use of loop diuretics is responsible for significant numbers of patients with Mg deficiency and hypomagnesemia. Life-threatening cardiac arrhythmias and seizures represent the most serious manifestations of clinical hypomagnesemia and Mg depletion. In the most critically ill patients, treatment with intravenous Mg is recommended. Oral repletion of Mg is reserved for the less critically ill hospitalized patients and ambulatory patients. Close attention must be paid to optimizing K replenishment in hypokalemic patients by concurrent treatment of any accompanying hypomagnesemia to avoid the problem of refractory K repletion. CONCLUSIONS: 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.

Arrhythmias, Cardiac↗
PubMed1979

Epileptic-type convulsions and magnesium deficiency.

Immediately following 4 h of continuous exercise at +/- 45% Vo2max in heat, a 23-year-old, well-trained man displayed epileptic-type convulsions. One week preceeding this incident, he completed an identical work test successfully under room temperature conditions. An assessment of his physiological and biochemical results indicated only one abnormality: during exercise in heat, an abnormally low serum magnesium concentration prevailed for most of the test. Treatment with phenobarb and magnesium chloride enteric tablets ("Slow Mag", 2 x 535 mg/d) reversed the biochemical abnormality. After checking his resting serum magnesium, the subject subsequently heat acclimatized and repeated similar treadmill tests as before without any ill effects.

Acclimatization↗
PubMed2006

Magnesium deficiency over generations in rats with special references to the pathogenesis of the Parkinsonism-dementia complex and amyotrophic lateral sclerosis of Guam.

Parkinsonism-dementia complex (PDC) and amyotrophic lateral sclerosis (ALS) are fatal neurological diseases. The incidence on Guam was very high between 1950 and 1965 but decreased dramatically after 1965. It is thought that drinking water containing low levels of calcium (Ca) and magnesium (Mg), and high levels of aluminum and of a plant excitatory neurotoxin are involved in the pathogenesis of these diseases. The present experiment was performed in rats that were exposed to low Ca and/or Mg intake over two generations, thus simulating the conditions of human life on Guam, where several generations live continuously in the same environment. Significant loss of dopaminergic neurons was identified exclusively in the substantia nigra in 1-year-old rats that had been exposed continuously to low Mg intake (one-fifth of the normal level) over generations. The present study suggests that low Mg intake over generations may be involved in the pathogenesis of substantia nigra degeneration in humans.

Amyotrophic Lateral Sclerosis↗
PubMed2006

Dietary magnesium deficiency decreases plasma melatonin in rats.

It has been postulated that Mg depletion is associated with decreased melatonin. Exogenous magnesium (Mg) has been found to increase the activity of serotonin N-acetyltransferase, an enzyme in the pathway for melatonin synthesis; but no data have been found on the effect of Mg deficiency on plasma melatonin. This pilot study examined the effect of a dietary Mg deficiency on plasma melatonin in male, Sprague-Dawley rats. Weanling rats were placed on a Mg-deficient (150 ppm) or a Mg-adequate (1000 ppm) diets for four weeks, after which they were sacrificed 4, 5 or 7 hours into the dark cycle. Plasma was assayed for melatonin concentrations. A significant decrease (p = 0.0101) occurred in mean (+/- SEM) plasma melatonin levels of the Mg-deficient animals (50 +/- 6.4 pg/mL) when compared to the Mg-adequate animals (75 +/- 6.6 pg/mL). There was no obvious phase shift in the melatonin profile of the Mg-deficient animals when compared to the Mg-adequate animals.

Animals↗