Magnesium and trace elements (Magnes Trace Elem )

Publisher: American Society for Magnesium Research


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    Magnesium and trace elements
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    ABSTRACT: Red blood (RBC) ionized magnesium (Mg2+) was determined by nuclear magnetic resonance (NMR) in order to assess the usefulness of this technique as an index of magnesium depletion. Twenty-four normal subjects underwent a 3-week low-Mg diet. The RBC Mg2+ fell from 209 +/- 9.8 microM before diet to 162 +/- 9.3 microM at the end of the 3 weeks (p < 0.001). In patient populations, 22 hypomagnesemic hospitalized patients had a significantly lower RBC Mg than normal (146 +/- 7.1 microM, p < 0.002), and 37 outpatients with diabetes mellitus had a mean RBC Mg2+ of 172 +/- 7.1 microM which was also significantly lower than normal (p < 0.001). These data suggest that determination of RBC Mg2+ may be used to reflect intracellular Mg status.
    Magnesium and trace elements 01/1993; 10(2-4):117-21.
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    ABSTRACT: The effect of acute ethanol perfusion on the intracellular free magnesium level, intracellular pH, and high energy phosphate levels of isolated adult rat hearts (n = 13) were studied using 31P nuclear magnetic resonance (NMR) spectroscopy. Perfusion with 1% ethanol solution resulted in a 43% decrease in the intracellular free magnesium level in Langendorff perfused rat hearts while intracellular pH was not significantly altered. In most hearts ethanol perfusion also resulted in increased intracellular inorganic phosphate and reduced phosphocreatine and ATP levels, corresponding to a significant reduction in phosphorylation potential. The implications of these results in the pathogenesis of alcohol-induced hypertension are discussed in light of our previous studies on spontaneously hypertensive and normotensive rats which demonstrated a correlation between cardiac free magnesium levels and blood pressure.
    Magnesium and trace elements 01/1993; 10(2-4):136-41.
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    ABSTRACT: The concentration of free Mg2+ in the matrix of isolated heart mitochondria has been monitored using the fluorescent probe furaptra. The techniques used for loading, calibrating and using furaptra fluorescence to monitor matrix free Mg2+ are described. Furaptra is loaded as the membrane-permeable acetoxymethyl ester which is hydrolyzed to the impermeant acid form by nonspecific esterases. Loading is sufficient in a 20-min period at 25 degrees C to give signals approximately 5-fold greater than nonloaded mitochondria. Uncertainties concerning the apparent dissociation constant value for Mg2+ for entrapped furaptra and the ability of ionophores to equilibrate Mg2+ across the mitochondrial membrane are discussed. We conclude that our best estimate for matrix Mg2+ in isolated mitochondria is 0.5 mM and that it can change significantly with changing Mg2+ ligand availability in the matrix.
    Magnesium and trace elements 01/1993; 10(2-4):151-64.
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    ABSTRACT: Magnesium, the second most abundant intracellular cation, is essential for life. The consequences of deficiency are severest in the smallest and youngest members of each species and may include sudden unexpected death. Magnesium deficiency, usually diagnosed by hypomagnesemia, may be congenital, as in premature infants, infants of magnesium-deficient mothers and infants with intrauterine growth retardation. It may be acquired or caused by low magnesium intake, the use of magnesium-wasting drugs, illness provoking gastrointestinal or renal losses of the mineral, or high metabolic demands imposed by catch-up growth or postsurgical healing. Finally, the deficiency may be conditioned, caused by excessive dietary calcium, phosphorus or protein in relation to dietary magnesium, especially during a period of rapid growth or tissue repair. Magnesium therapy is safe when a low dosage is given with monitoring of plasma or serum magnesium levels, with occasional checking of calcium and potassium levels. A parenteral dose of 0.1 ml/kg/day of 50% magnesium sulfate USP (approx. 0.2 mmol/kg/day or 0.4 mEq/kg/day) may be given for 5 dose days. An oral dose of 1.0 ml of 10% magnesium chloride solution providing 0.5 mmol/kg/day magnesium or 1.0 ml/kg/day of 10% magnesium chloride USP (0.5 mmol/kg/day) or magnesium magonate (Magonate) 1.0 ml/kg/day (0.45 mmol/kg/day) may be given for extended periods; higher doses may be required for malabsorption syndromes. Hypermagnesemia, which usually results from magnesium overdosage or inadequate renal function, is a potential threat to neonates born to magnesium-treated eclamptic mothers. Most show marked improvement after 36 h of conservative management that includes calcium salts and intravenous infusions of glucose and saline, but obtunded neonates may require dialysis.
    Magnesium and trace elements 01/1993; 10(2-4):229-50.
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    ABSTRACT: The development of fluorescent ion-selective indicators for magnesium has provided valuable tools for measuring second-by-second changes in cytosolic magnesium activity. In the course of establishing appropriate protocols for using one of these indicators, mag-fura-2, to measure magnesium activity in BC3H-1 cells and chick ventricular myocytes, many potential pitfalls and limitations of this technique have been encountered and addressed. These observations are presented for the purpose of providing guidelines regarding the appropriate use of this indicator and on factors influencing the interpretation of resulting data.
    Magnesium and trace elements 01/1993; 10(2-4):142-50.
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    ABSTRACT: The magnesium content of the adult human is approximately 24 g (1 mol), about half lies in bone and half in soft tissue. Less than 1% of the total body magnesium is present in blood, with approximately 0.3% present in serum. Total magnesium has been determined in several body tissues, but we lack information about free magnesium, which has physiologic significance. Current assessment of magnesium status is difficult as there is no simple, rapid and accurate test(s) to indicate total body magnesium status. I discuss 12 tests in three functional categories that have been used clinically or in research to assess magnesium status. Determining total magnesium in tissues and physiologic tests may provide important information. A test for the routine determination of free magnesium in serum should improve the assessment of magnesium status. A combination of available tests is recommended.
    Magnesium and trace elements 01/1993; 10(2-4):172-81.
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    ABSTRACT: Ion-sensitive microelectrodes (ISEs) have been used to measure intracellular [Mg2+] ([Mg2+]i) in cardiac muscle, although most measurements have tended to overestimate the value due to the poor selectivity of the Mg2+ ionophore in the sarcoplasm and to inaccurate collation of individual ISE measurements. This paper highlights the correct method for analysis of data from multiple ISE experiments. Since [Mg2+]i is constrained at a lower concentration than would be expected by passive distribution of the ion, some of the possible mechanisms underlying Mg2+ extrusion from ferret ventricular myocardium were investigated. During elevation of the extracellular [Mg], mean [Mg2+]i rose from 1.61 to 1.91 mM. The same intervention had no significant effect on membrane potential, intracellular [Na+] or pH measured with ISEs, and there was no change in resting [Ca2+], as assessed from fura-2 fluorescence. The data are not consistent with a simple mechanism for Na(+)-Mg2+ exchange as the primary mode of Mg2+ regulation in cardiac muscle or with an Mg2+ extrusion mechanism involving steady-state ion exchange.
    Magnesium and trace elements 01/1993; 10(2-4):80-9.
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    ABSTRACT: The reference system, preanalytical variables, specimen requirements and methodology for determination of magnesium in serum by clinical laboratories are discussed. Most clinical laboratories determine the serum magnesium concentration by colorimetric methods. Four different chromophores (calmagite, methylthymol blue, formazan dye and magon) are commonly used for the determination of serum magnesium on automated instruments by clinical laboratories. The College of American Pathologists Proficiency Testing Survey shows that instruments using the chromophore magon have a larger coefficient of variation among laboratories than most instruments using a different chromophore.
    Magnesium and trace elements 01/1993; 10(2-4):60-6.
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    ABSTRACT: Magnesium has a profound effect on neural excitability; the most characteristic signs and symptoms of Mg deficiency are produced by neural and neuromuscular hyperexcitability. These create a constellation of clinical findings termed tetany syndrome (TS). TS symptoms include muscle spasms, cramps and hyperarousal, hyperventilation and asthenia. Physical signs (Chvostek's, Trousseau's or von Bonsdorff's) and abnormalities of the electromyogram or electroencephalogram can usually be elicited. Signs and symptoms of TS are frequently encountered in clinical practice, especially among patients with functional or stress-related disorders. The role of Mg deficit in TS is suggested by relatively low levels of serum or erythrocyte Mg and by the clinical response to oral Mg salts, which has been demonstrated in controlled studies. Among the more serious neurologic sequelae of TS are migraine attacks, transient ischemic attacks, sensorineural hearing loss and convulsions. Mg deficiency may predispose to hyperventilation and may sensitize the cerebral vasculature to the effects of hypocarbia. Mg deficiency increases susceptibility to the physiologic damage produced by stress, and Mg administration has a protective effect; studies on noise stress and noise-induced hearing loss are taken as an example. In addition, the adrenergic effects of psychological stress induce a shift of Mg from the intracellular to the extracellular space, increasing urinary excretion and eventually depleting body stores. Drugs used in neurology and psychiatry may affect Mg levels in blood and may diminish signs of tetany, making assessment of Mg status more difficult. Pharmacologic use of Mg can decrease neurologic deficit in experimental head trauma, possibly by blockade of N-methyl-D-aspartate receptors. In conjunction with high doses of pyridoxine, Mg salts benefit 40% of patients with autism, possibly by an effect on dopamine metabolism.
    Magnesium and trace elements 01/1993; 10(2-4):287-301.
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    ABSTRACT: The cellular bioenergetic responses of isolated perfused working rat hearts to alterations in hemodynamic function caused by acute exposure to elevated levels of extracellular magnesium ions ([Mg2+]o) were examined using 31P nuclear magnetic resonance (31P NMR) spectroscopy. Results showed that in hearts working against 90 cm H2O afterload, an increase in [Mg2+]o from 1.2 to 4.8 mM reduced the heart rate by 35%, while coronary flow was increased by 38%. Unexpectedly, despite the pronounced bradycardia, the rate-pressure product was reduced only slightly (from 2.36 x 10(4) to 2.08 x 10(4) mm Hg/min) due to a significant increase (36%) in systolic pressure. In addition, cardiac output actually increased by 23%, owing to a > 100% increase in stroke volume, indicating that the performance of the heart was improved and suggesting that the efficiency of the heart was improved as well. In a separate series of experiments, 31P NMR measurements performed on hearts perfused in the Langendorff mode revealed that elevated levels of [Mg2+]o increase phosphocreatine (PCr) levels by 23% (from 9.2 to 11.3 mM), while Pi levels declined by a corresponding amount. Perfusion of hearts in the working mode with elevated [Mg2+]o was also observed to increase PCr levels from 6.3 to 9.0 mM, while ATP levels declined by 17%. Measurement of the chemical shift difference between Pi and PCr and that between the alpha and beta phosphate resonances of ATP were used to determine intracellular pH and the cytosolic levels of free Mg2+ ([Mg2+]i), respectively. These results showed that acute exposure of hearts, perfused in either the working or Langendorff mode, to increased levels of [Mg2+]o increased intracellular pH by 0.12-0.13 units, while free Mg2+ nearly doubled to a level of 1.1-1.2 mM. The latter observation may suggest that acute variations in the level of [Mg2+]o can influence a multitude of cellular processes requiring Mg2+ as an essential cofactor. Using the above data and assuming equilibrium of the creatine kinase reaction, the levels of ADP, cytosolic phosphorylation potential ([ATP]/[ADP][Pi]) and free energy change from ATP hydrolysis (-delta G/delta E) were also calculated. Results obtained illustrate that in the presence of elevated [Mg2+]o, ADP levels declined by 33-48%, the cytosolic phosphorylation potential increased from 41 to 112 mM-1 and -delta G/delta E increased from 56.7 to 59.3 kJ/mol. These changes are not completely accountable by the known bradycardia and vasodilatory effects of elevated [Mg2+]o and strongly argue for a direct action of [Mg2+]o on the myocyte as well.(ABSTRACT TRUNCATED AT 400 WORDS)
    Magnesium and trace elements 01/1993; 10(2-4):99-116.
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    ABSTRACT: Diagnostic categories that are useful for describing patients with acute or organ failure disease are generally less useful labels for primary care and preventive medicine patients whose conditions are better described by signs and symptoms. Symptoms may be clues to ill health but are not often criteria for a major diagnostic labeling. In my practice I have used a computer-based medical record system that permits portrayal and comparison of symptom data to correlate varying degrees of retention of an intramuscular magnesium-loading study (IMMLS) with symptom patterns in 172 patients. The group of patients who show a paradoxical excretion of more Mg than they were given in the IMMLS are a distinctive group with lower blood pressures and significantly fewer digestive and skin symptoms, fewer symptoms of inflammation but more emotional symptoms than those with normal Mg excretion. The group who retained > 49% of the load had higher blood pressures and significantly fewer symptoms of inflammation of the skin and of the reproductive tract.
    Magnesium and trace elements 01/1992; 10(2-4):251-62.
  • Magnesium and trace elements 01/1992; 10:182-192.
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    ABSTRACT: We have previously established a link between magnesium-deficiency-induced cardiomyopathy and free radical injury. In the present study, golden Syrian male hamsters were placed on either magnesium-deficient or magnesium-supplemented diets. Animals from each group received either d,l-propranolol or d-propranolol (the non-beta-blocking form). After 14 days, the animals were sacrificed and their hearts isolated for morphological and morphometric analyses. Hematoxylin/eosin-stained sections were examined by a computer image analysis system for a morphometric determination of the severity of myocardial injury. Propranolol reduced both the density of lesions, from 0.32 to 0.06 lesions/mm2 (p < 0.01), and the area fraction of lesions, from 9.8 x 10(-4) to 2.5 x 10(-4) lesion area/mm2 (p < 0.01). In addition, d-propranolol was virtually equipotent to d,l-propranolol, indicating that part of the protective effect of propranolol, in this model, was attributable to its antioxidant properties.
    Magnesium and trace elements 01/1991; 10(5-6):348-54.
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    ABSTRACT: The following study was conducted to assess the biochemical and nutritional status of new military recruits during 12 weeks of strenuous physical activity. Calorie and magnesium (Mg) intake, energy expenditure, and serum, red blood cell (RBC) and mononuclear cell (MNC) Mg were assessed at the start, after 6 weeks and after 12 weeks of training. The results provide evidence that MNC Mg content decreases, whereas serum Mg increases, under prolonged, strenuous training conditions in previously unconditioned military recruits. Mg dietary intake alone could not account for these changes. It is postulated that this decrease in MNC Mg (from 64.76 +/- 34.99 to 23.81 +/- 15.55 fg/cell), unparalleled by similar changes in serum Mg or RBC Mg, reflects a reduction in exchangeable Mg body stores, and the onset of a Mg deficiency state.
    Magnesium and trace elements 01/1991; 10(5-6):420-6.
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    ABSTRACT: The efficacy of oral magnesium supplementation in correcting magnesium deficiency was examined in a group of 40 elderly patients with suspected magnesium deficiency. The patients were randomized in a double-blind, placebo-controlled fashion to oral magnesium-lactate-citrate for 6 weeks. Magnesium status was assessed by an intravenous magnesium-loading test at baseline and after treatment. For comparison, another group of 23 patients received 30 mmol magnesium sulfate intravenously daily for 7 days. A group of 30 patients without known predisposition to magnesium deficiency and a group of 27 young healthy subjects served as controls. The initial magnesium-loading test in the placebo group reduced magnesium retention from a mean 41% (95% confidence intervals 34-49) to 22% (15-29) (p less than 0.01). In the group receiving oral magnesium supplementation for 6 weeks, magnesium retention decreased from 39% (31-47) to 10% (2-18) (p less than 0.01), which was significantly better than with placebo treatment (p less than 0.01). The magnesium retention after oral magnesium supplementation was comparable to that observed after parenteral administration of magnesium for 7 days, 6% (-4 to 16), and to that in the reference groups of patients 4% (-2 to 10) and healthy control subjects 3% (-2 to 8). The study suggests that the bioavailability of orally given magnesium-lactate-citrate is satisfactory, and that oral administration of magnesium for 6 weeks may restore magnesium depots in patients with magnesium deficiency.
    Magnesium and trace elements 01/1991; 10(1):11-6.
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    ABSTRACT: The urinary excretion of magnesium was studied in two groups of healthy women just after menopause. The women in group I were randomly allocated to receive either placebo or 4, 2 or 1 mg 17 beta-oestradiol in cyclical combination with 1 mg norethisterone acetate (a progestational agent). Oestradiol was given, in the above-mentioned doses, from days 1 to 22, and 1, 1 or 0 mg oestradiol was given from days 23 to 28, in combination with norethisterone acetate from days 13 to 22 and oestriol 2, 1 or 0.5 mg from days 1 to 23 and 0.5, 0.5 or 0 mg from days 23 to 28. The women in group II were allocated to receive either placebo, 2 mg oestradiol valerate in cyclical combination with 1 mg cyproterone acetate (oestradiol valerate from days 1 to 21 and cyproterone acetate from days 12 to 21) with 1,000 mg of calcium per day or oestradiol valerate + cyproterone acetate without calcium. Oestrogen and progesterone therapy decreased the urinary magnesium excretion significantly when compared to the placebo group. The effect was related to the dose of oestrogen. Furthermore, our results indicate that calcium supplementation influences the urinary excretion of magnesium in a two-phase paradoxical manner.
    Magnesium and trace elements 01/1991; 10(1):34-9.
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    ABSTRACT: Dietary boron, in concentrations similar to that found in human diets comprised mainly of fruits and vegetables, affects both mineral and energy metabolism. Therefore, the effects of boron on a model system with a perturbed metabolic insulin-vitamin D3 axis was examined. Weanling male rats were fed a ground corn-high protein casein-corn oil-based diet (0.06 mg B/kg; no supplemental vitamin D3) supplemented with B (as orthoboric acid) at 0 or 2.4 mg/kg. After 55 days, all rats were equilibrated in individual metabolic cages for 6 days. After another 6 days, one half of the rats in both dietary groups were injected intraperitoneally with streptozotocin (STZ). All rats were killed 3 days after STZ treatment. STZ affected many aspects of mineral metabolism as expected. Plasma ionized calcium concentrations fell by approximately 10% in STZ-treated rats. Brain and heart mineral metabolism was spared from the toxic effects of STZ whereas spleen mineral metabolism was especially vulnerable to STZ. Supplemental dietary boron increased urinary excretion of calcium in the non-STZ rats but did not affect the plasma concentrations of alkaline phosphatase, ionized calcium or the concentration of calcium in the brains, lungs, kidneys and spleens of those animals. Supplemental dietary boron temporarily reduced the abnormally elevated renal excretion of albumin, potassium and sodium during the acute phase of diabetes mellitus. On the other hand, physiological amounts of dietary boron exacerbated the abnormally elevated rate of collagen breakdown in the STZ animal. Finally, boron may have indirectly affected heart mineral metabolism because dietary boron did not affect cardiac boron concentrations but did affect cardiac copper, calcium, manganese, molybdenum and phosphorus concentrations, primarily in non-STZ rats. The findings suggest that dietary boron has both protective and regulatory roles in mineral metabolism.
    Magnesium and trace elements 01/1991; 10(5-6):387-408.
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    ABSTRACT: In 25 full-term infants at birth and in their mothers, we determined plasma and mononuclear blood cell (MBC) Mg levels in order to investigate the relationship between maternal and fetal Mg status. MBC isolation for Mg analysis was carried out with a Ficoll-Isopaque gradient which is commercially available in disposable tubes. There was no difference in the plasma and MBC Mg levels between infants and their mothers. Neonatal MBC Mg content was significantly correlated with maternal plasma Mg concentration. The data demonstrate that MBC Mg content does not present any difference on the basis of age and emphasize that the constitution of fetal Mg reserve depends on maternal plasma Mg concentration.
    Magnesium and trace elements 01/1991; 10(1):30-3.
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    ABSTRACT: Nuclear magnetic resonance (NMR) studies of central nervous system (CNS) trauma have shown that intracellular free magnesium (Mg) concentration declines following injury. This fall in free Mg concentration was associated with a decrease in brain total tissue Mg concentration. Declines in both free and total tissue Mg concentration could be prevented or attenuated by treatments targeted to improve neurologic outcome by inhibition of specific injury factors, such as excitatory amino acids and opioid peptides. Furthermore, the extent of these changes in CNS Mg concentration and their attenuation with a diversity of treatments have been correlated to neurologic outcome. As such, it has been proposed that Mg, and in particular the cytosolic free Mg concentration, plays a critical central role in determining the degree of neurologic deficit expressed following a traumatic injury to the CNS. This mini-review will focus on the evidence suggesting that Mg concentration is important in the development of irreversible tissue damage following traumatic brain injury, and will discuss the relative importance of Mg to this process, and its interrelationship with a number of other proposed injury factors.
    Magnesium and trace elements 01/1991; 10(1):1-10.
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    ABSTRACT: Although alcohol has long been known to induce cardiac depression and cardiomyopathy, it is not known whether drug therapy or pharmacologic manipulation can be used to prevent or reverse these toxicities. With this in mind, high levels (15 mM) of magnesium (Mg) were investigated for their potential antialcohol effects on perfused rat hearts. A high concentration of ethanol (135 mM) was used to induce rapid cardiac failure as assessed by hemodynamic and metabolic parameters. During ethanol perfusion in normal 1.2 mM [Mg2+]o physiologic salt solution, coronary flow decreased immediately, and all of the hemodynamic parameters studied (except for heart rate) were depressed significantly. After 10 min of 135 mM ethanol perfusion, only 60% of the hearts kept beating; at 15 min, only 42% of the hearts continued to beat. Myocardial metabolism under such conditions as assessed by examination of coronary effluent concentrations of lactic acid (LA), lactic acid dehydrogenase (LDH) and creatine phosphokinase (CPK) was rapidly and severely compromised. Although 15 mM MgSO4 alone did not alter coronary flow and systolic pressure under the conditions studied, it did decrease cardiac output, heart rate and total pressure developed. However, when 15 mM MgSO4 was given 10 min before ethanol, and continued during ethanol perfusion, the usual depression in all assessed cardiac hemodynamic parameters (except heart rate) caused by ethanol was not observed. During 15 min of high [Mg2+]o perfusion, coronary flow recovered from 19.1 +/- 6.8% (ethanol alone) to 68.1 +/- 9.9% of control values (p < 0.01); cardiac output recovered from 10.4 +/- 4.6% (ethanol alone) to 43.6 +/- 7.5% of control (p < 0.01); stroke volume went from 12.9 +/- 5.8% (ethanol alone) to 97.1 +/- 14.5% of control (p < 0.01); systolic pressure from 55.3 +/- 3.6% (ethanol alone) to 88.8 +/- 4.0% of control (p < 0.01), and total pressure developed from 23.9 +/- 7.8% (ethanol alone) to 35.0 +/- 4.5% of control (p < 0.05). Assessment of the metabolic biochemical parameters supported these changes in hemodynamic improvement. For example, LA, LDH and CPK all went from elevated values towards normal levels. There were similar hemodynamic and metabolic responses to high [Mg2+]o given during ethanol perfusion to that given before ethanol perfusion. The hemodynamic and metabolic beneficial effects between groups pretreated or treated with high [Mg2+]o exhibited no significant differences. These results suggest that high [Mg2+]o (15 mM) given either before or during ethanol-induced cardiotoxicity is effective in attenuating both functional and metabolic damage caused by high ethanol perfusion in the rat heart.
    Magnesium and trace elements 01/1991; 10(5-6):409-19.