SEARCH · Search PubMed

Results for “MAGNESIUM”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

SourceResearch connectionFrom yearThrough year

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 181 records · Page 10Linked to original sources

PubMed1993

Oral magnesium supplementation restores the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle of patients receiving diuretic treatment.

In 76 consecutive patients who had received diuretics for 1-17 years for arterial hypertension or congestive heart failure, muscle concentrations of magnesium, potassium, and sodium-potassium pumps were significantly reduced compared to 31 age- and sex-matched controls. Thirty-six patients with muscle magnesium and/or potassium below the control level received oral magnesium hydroxide supplement for 2-12 weeks (n = 20) or 26 weeks (n = 16). After short-term (2-12 weeks) magnesium supplementation muscle parameters were increased, but far from normalized. After magnesium supplementation for 26 weeks, the muscle concentrations of magnesium, potassium and sodium-potassium pumps were normalized in most cases. Oral magnesium supplementation may restore diuretic-induced disturbances in the concentrations of magnesium, potassium and sodium potassium pumps in skeletal muscle. A supplemental period of at least 6 months seems to be required before complete normalization can be expected.

Administration, Oral↗

PubMed1992

Failure of magnesium supplementation to influence marathon running performance or recovery in magnesium-replete subjects.

This study examined the effect of magnesium supplementation on muscle magnesium content, on running performance during a 42-km marathon footrace, and on muscle damage and the rate of recovery of muscle function following the race. Twenty athletes were divided equally into two matched groups and were studied for 4 weeks before and 6 weeks after a marathon in a double-blind trial; the experimental group received magnesium supplement (365 mg per day) and the control group, placebo. Magnesium supplementation did not increase either muscle or serum magnesium concentrations and had no measurable effect on 42-km marathon running performance. Extra magnesium ingestion also had no influence on the extent of muscle damage or the rate of recovery of muscle function. The latter was significantly reduced immediately after the marathon but returned to normal within 1 week. Thus, magnesium supplementation in magnesium-replete subjects did not enhance performance or increase resistance to muscle damage during the race, or the rate of recovery of muscle function following the race.

Adult↗

PubMedDate not supplied

Magnesium and thermoregulation. I. Newborn and infant. Is sudden infant death syndrome a magnesium-dependent disease of the transition from chemical to physical thermoregulation?

The sudden infant death syndrome (SIDS) remains a leading cause of death during the first year. The common epidemiological and pathological data which characterize SIDS include the curve for age at death (with 3 months as modal age), the stigmata of early maternal intrauterine injury, the seasonal predominance in winter, and the absence of an adequate cause of death at autopsy. Some data characterize risk factor subgroups: for example low socioeconomic level, environmental pollution, stress, and mistakes in baby care. Symptoms before death may be lacking, they may be common and non-specific, or rarely they may be acute, corresponding to "apparent life-threatening events" (ALTE). SIDS may be a magnesium-dependent disease of the transition from chemical to physical thermoregulation. This theory originates from a synthesis of our present knowledge of SIDS, maternal magnesium status, and thermoregulation in the baby. It is consistent with all the epidemiological and pathological prerequisites characterizing SIDS. It eliminates the hiatus between relatively minor thermal stress and induced lethal thermal stroke. Logical scepticism about the role of an implausible lethal superacute magnesium deficiency is no longer justified with regard to well established chronic marginal magnesium deficiency. Further experimental and clinical research will be interesting, i.e. ex vivo studies on brown adipose tissue (BAT) and magnesium deficiency under various conditions of thermal exposure. But even now the theory leads to three therapeutic consequences: (1) the need to define the importance of magnesium deficiency in diagnosis and treatment of ALTE; (2) an assessment of the use of new techniques of rewarming (i.e. extracorporeal circulation) in hypothermia cases to distinguish cot death from "apparent death"; (3) investigation of the prevention of SIDS with magnesium through a blinded and randomized multicentre prospective cooperative study of magnesium supplementation in pregnant and lactating women, followed not only in the mother, fetus, and neonate at birth, but also through the first year of life.

Body Temperature Regulation↗

PubMed1994

[Oral magnesium supplementation to patients receiving diuretics--normalization of magnesium, potassium and sodium, and potassium pumps in the skeletal muscles].

In 76 consecutive patients who had received diuretics for 1-17 years for arterial hypertension or congestive heart failure, muscle concentrations of magnesium, potassium, and sodium-potassium pumps were significantly reduced compared to 31 age- and sex-matched controls. Thirty-six patients with muscle magnesium and/or potassium below the control level received oral magnesium hydroxide supplement for 2-12 weeks (N = 20) or 26 weeks (N = 16). After short term (2-12 weeks) magnesium supplementation muscle parameters were increased, but far from normalized. After magnesium supplementation for 26 weeks, the muscle concentrations of magnesium, potassium and sodium-potassium pumps were normalized in most cases. Oral magnesium supplementation may restore diuretic-induced disturbances in the concentrations of magnesium, potassium and sodium-potassium pumps in skeletal muscle. A supplemental period of at least six months seems required before complete normalization can be expected.

Administration, Oral↗

PubMed1996

Complementary vascular-protective actions of magnesium and taurine: a rationale for magnesium taurate.

By a variety of mechanisms, magnesium functions both intracellularly and extracellularly to minimize the cytoplasmic free calcium level, [Ca2+]i. This may be the chief reason why correction of magnesium deficiency, or induction of hypermagnesemia by parenteral infusion, exerts antihypertensive, anti-atherosclerotic, anti-arrhythmic and antithrombotic effects. Although the amino acid taurine can increase systolic calcium transients in cardiac cells (and thus has positive inotropic activity), it has other actions which tend to reduce [Ca2+]i. Indeed, in animal or clinical studies, taurine lowers elevated blood pressure, retards cholesterol-induced atherogenesis, prevents arrhythmias and stabilizes platelets--effects parallel to those of magnesium. The complex magnesium taurate may thus have considerable potential as a vascular-protective nutritional supplement, and might also be administered parenterally, as an alternative to magnesium sulfate, in the treatment of acute myocardial infarction as well as of pre-eclampsia. The effects of magnesium taurate in diabetes deserve particular attention, since both magnesium and taurine may improve insulin sensitivity, and also may lessen risk for the micro- and macrovascular complications of diabetes.

Animals↗

PubMed1976

Magnesium, calcium and zinc levels of maternal and fetal tissues in magnesium deficient rats.

The interaction of magnesium with two other mineral elements, calcium and zinc, was studied in maternal tissues and fetuses of pregnant rats fed a magnesium deficient diet throughout gestation. Reduction in maternal femur magnesium and a trend for increased kidney calcium reflected the dietary magnesium deficiency. In fetuses, however, total magnesium content was reduced and , in addition, fetal zinc content was also lower than normal in the group most severly deficient in magnesium. The possible interpretation of this magnesium-zinc interaction is discussed.

Animals↗

PubMed1982

Magnesium requirement of fingerling channel catfish and signs of magnesium deficiency.

Purified casein diets with and without supplemental magnesium were fed to fingerling channel catfish (Ictalurus punctatus) in order to establish the essentially of this mineral. Fish fed the basal diet containing 0.004% magnesium developed deficiency signs such as poor growth, anorexia, sluggishness, muscle flaccidity and high mortality. After 3 weeks, two groups of fish fed the basal diet were converted to the supplemental diet containing 0.057% magnesium. Deficiency signs in these fish were alleviated almost immediately. In a second experiment, graded levels of magnesium sulfate were added to casein-based diets and fed to channel catfish fingerlings to determine their dietary requirement for magnesium. Results indicated that a minimum magnesium level of 0.04% of the dry diet was required to maintain normal growth, serum and bone magnesium levels in channel catfish fingerlings.

Animals↗

PubMed1995

Insulin increases renal magnesium excretion: a possible cause of magnesium depletion in hyperinsulinaemic states.

The effects of insulin upon renal magnesium excretion were examined. Urinary magnesium excretion rates were measured in seven healthy volunteers (three men, four women) before and during a euglycaemic, hyperinsulinaemic clamp. Insulin was infused at 120 pmol m-2 min-1 and at 240 pmol m-2 min-1. Compared to baseline, the renal magnesium excretion increased 30% during the infusion of insulin at a rate of 120 pmol m-2 min-1. During infusion of insulin, 240 pmol m-2 min-1, renal magnesium excretion increased 50% compared to baseline. There were no changes in either glomerular filtration rates, plasma magnesium, urinary volume or general changes in the renal handling of divalent ions as judged by an unchanged urinary excretion rate of calcium (0% during infusion of insulin, 120 pmol m-2 min-1, and 8% increase during infusion of 240 pmol m-2 min-1 (NS). During the 120 pmol m-2 min-1 insulin infusion rate, plasma insulin rose from 46.1 pmol I-1 to 158.8 pmol I-1 and during the 240 pmol m-2 min-1 insulin infusion rate, mean plasma insulin concentration was 361.4 pmol I-1. Thus, physiological concentrations of insulin induce a specific increase in the renal excretion of magnesium. This might partly explain the magnesium depletion observed in various hyperinsulinaemic states, diabetes mellitus, atherosclerosis, hypertension, and obesity.

Adult↗

PubMed1998

The effect of varying molar ratios of potassium-magnesium citrate on thiazide-induced hypokalemia and magnesium loss.

This study was conducted to compare the value of an older formulation of potassium-magnesium citrate (K4MgCit2) with newer formulations (K3MgHCit2 and K5MgCit2Cl) with respect to the correction of thiazide-induced hypokalemia and magnesium loss, alkalinizing effect, and citraturic action. Sixty-two healthy volunteers first took hydrochlorothiazide 50 mg/day. After 3 weeks of thiazide treatment (or earlier if hypokalemia developed), they were randomized to take one of three drugs for 3 weeks while continuing thiazide: K4MgCit2 (49 mEq K, 25 mEq Mg, and 74 mEq citrate/day), K3MgHCit2 (49 mEq K, 33 mEq Mg, and 98 mEq citrate/day), and K5MgCit2Cl (49 mEq K, 20 mEq Mg, 10 mEq Cl and 59 mEq citrate/day). Outcome measures were changes in serum potassium and magnesium, and urinary potassium, magnesium, pH, and citrate. The three drugs were equally effective in correcting thiazide-induced hypokalemia. K3MgHCit2 and K4MgCit2 produced a small but significant increase in serum magnesium concentration, whereas K5MgCit2Cl did not. Although all three supplements significantly increased urinary pH and citrate, these effects were more marked with K3MgHCit2 and K4MgCit2 than with K5MgCit2. All three supplements were generally well tolerated, with the lowest side effect profile obtained with K4MgCit2. The new formulation of K3MgHCit2 exerts similar correction of thiazide-induced hypokalemia and magnesium loss, and enhancement of urinary pH and citrate, compared with the older K4MgCit2. However, it is less well tolerated. The new formulation of K5MgCit2Cl does not avert magnesium loss, and has less prominent alkalinizing and citraturic effects than the older preparation.

Adult↗

PubMed1983

Effect of supplemented magnesium from magnesium oxide or dolomitic limestone upon digestion and absorption of minerals in sheep.

Three metabolism trials were conducted with six lambs fitted with abomasal and ileal cannulae to determine the site of supplemental Mg absorption when supplied as dolomitic limestone or magnesium oxide. Magnesium intake was 1.09 g/d for the lambs fed the control diet and 2.21 and 2.10 g for those fed the dolomitic limestone and magnesium oxide supplemented diets, respectively. Irrespective of its source, the major site of Mg absorption was the preintestinal region. Magnesium was secreted in the small intestine in lambs fed all three diets. Magnesium supplementation resulted in an increase (P less than .05) in preintestinal Mg absorption, with magnesium oxide having the highest value. Supplementation had no effect (P greater than .05) on secretion or absorption of Mg from the small and large intestines or total retention of Mg. With all three diets, the major site of Ca absorption was the stomach region with additional absorption taking place in the large intestine. Calcium was secreted in the small intestine of lambs fed all treatments. Generally, K, Na and P were secreted in the preintestinal region and absorbed from the small and large intestines. The major site of K and P absorption appeared to be the small intestine and for Na, the large intestine. Serum minerals were unchanged (P greater than .05) due to treatment, but the levels of Mg, K and inorganic P tended to be higher in lambs supplemented with either of the Mg sources. It appears that the greater utilization of Mg from magnesium oxide vs dolomitic limestone is due to greater absorption of Mg from the forestomach region.

Animals↗

PubMed1998

[Study of magnesium and calcium levels of plasma and within erythrocyte before and after magnesium sulfate treatment in patients with pregnancy induced hypertension].

OBJECTIVE: To study the changes of calcium and magnesium levels in patients with pregnancy induced hypertension (PIH) and the therapeutic effect of magnesium sulfate (MgSO4). METHODS: The calcium and magnesium levels in plasma and erythrocytes of 36 patients with PIH and 14 healthy gravidi in their late pregnancy were determined and the changes after 4 hours infusion of MgSO4 as well. RESULT: Plasma calcium decreased significantly in moderate and severe PIH patients, but calcium increased and magnesium decreased in their erythrocytes. After MgSO4 infusion for PIH, magnesium levels in both plasma and erythrocytes increased, while calcium increased in plasma and decreased in erythrocyte to normal levels. CONCLUSION: Magnesium deficiency is the basis of calcium and magnesium disturbances in PIH, and MgSO4 treatment may improve the situation effectively.

Adolescent↗

PubMed1981

Urinary magnesium, calcium, and phosphate excretion during magnesium sulfate infusion.

Urinary excretion of magnesium, calcium, and phosphate was measured in 20 preeclamptic pregnant women treated with intravenous magnesium sulfate. Blood levels of these substances, as well as of parathyroid hormone and calcitonin, were also measured. Urinary magnesium excretion increased 20-fold during magnesium sulfate infusion. Seventy-five percent of the infused magnesium was excreted during the infusion, and 90% within 24 hours after treatment. Urinary calcium concentration increased 4.5-fold during magnesium sulfate infusion, and the urinary calcium excretion rate was 3 times that observed in controls. Urinary phosphate concentration and excretion rate were the same in treated and control subjects. During treatment, maternal serum total calcium fell 25%, ionized calcium fell 12%, and parathyroid hormone rose 26%. Magnesium sulfate therapy depresses maternal calcium levels by increasing urinary calcium loss, and increased parathyroid hormone output prevents more marked hypocalcemia.

Calcitonin↗

PubMed1997

[Comparative study of the short-term acceptability and tolerance of a new oral formulation of magnesium (TX 1341) and a reference magnesium].

This open, randomized study on 2 parallel groups compared the acceptability, digestive tolerance and observance of TX 1341, a new chewable magnesium tablet (OROMAG, Laboratoire Théramex) to that of a reference magnesium (MAG2, Laboratoire Théraplix). 179 patients warranting a magnesotherapy were treated for 10 weeks either by 3 chewable lactate and citrate of magnesium tablets (TX 1341) each containing 120 mg of magnesium-element, or by 3 drinkable ampoules of pidolate of magnesium (each of 122 mg of magnesium-element). Acceptability was assessed at the end of the study by a semi-quantitative scale at four levels and digestive tolerance by closed questionnaire submitted before and after treatment. 72.7% of patients treated by TX 1341 find the treatment agreeable against 46.1% with the reference magnesium (p < 0.01). The number of drops out linked to treatment is not significantly different in the two groups and they are virtually all linked to digestive problems. The two medications significantly lower the number of cases of constipation without noticeably increasing the number of cases of diarrhea. The comparison of the number of digestive symptoms which appeared under treatment only underline one significant difference between the 2 groups (p < 0.05): the appearance of 5 times less the number of abdominal pains with TX 1341 (2 cases). Cases of irregular intake are significantly higher with the reference drug than with TX 1341 (respectively 23.7% and 8.5%; p < 0.01).

Administration, Oral↗

PubMed1986

Magnesium and acute myocardial infarction. Transient hypomagnesemia not induced by renal magnesium loss in patients with acute myocardial infarction.

Serum magnesium concentrations and the rate of urine magnesium excretion were studied in 24 patients with suspected acute myocardial infarction (AMI). Blood and urine samples were taken on admission, at three-hour intervals for the first 24 hours after admission, and every eight hours for the next 24 hours. Thirteen of the patients were found to have AMI, and the 11 who did not have AMI served as a control. During the first 32 hours, the AMI group had significantly low serum magnesium concentrations. The serum magnesium concentrations were unchanged in the control group. Results of the urine samples disproved our hypothesis that the drop in serum magnesium concentrations was due to an increased renal magnesium loss. These results indicate a magnesium migration associated with AMI, from extracellular to intracellular space.

Adult↗

PubMed1999

Some magnesium salts and a mixture of magnesium and calcium salts accelerate skin barrier recovery.

The effects of four different magnesium salts on the cutaneous barrier recovery rate after barrier disruption were evaluated. We spread an aqueous solution of each salt on the flank skin of hairless mice, occluded the area with a plastic membrane for 20 min, and then left the skin surface to dry. All of the magnesium salts, except magnesium bis(dihydrogen phosphate), accelerated barrier repair. We next estimated the effects of magnesium chloride aqueous solutions which contained calcium chloride at different molar ratios. When the calcium to magnesium ratio was lower than 1, the mixture accelerated barrier repair. The application of an aqueous solution of 10 mM magnesium chloride and 10 mM calcium chloride was found to hasten the barrier recovery more effectively than a solution of 10 mM magnesium chloride. These results suggest that the effects of these metal ions are different depending on the counter ion and/or the method of application.

Animals↗

PubMed1991

Relationship between total magnesium concentration and free intracellular magnesium in sheep red blood cells.

The cellular free magnesium concentration of ionophore A23187 permeabilized high potassium sheep erythrocytes was measured by 31P nuclear magnetic resonance spectroscopy, and the total cellular magnesium concentration was determined by atomic absorption spectroscopy. The free versus total cellular magnesium concentrations yield a linear relationship on a log-log scale in the concentration range from 0.3 to 1.92 mmol Mg/liter cells. Thus, free intracellular magnesium concentrations can be calculated from atomic absorption data. The method permits the estimation of physiologically or experimentally induced variations of intracellular free magnesium concentrations between 7 and 405 microM magnesium in cell water. This range encompasses the free magnesium concentration of 335 +/- 60 microM in cell water determined for untreated erythrocytes.

Adenosine Triphosphate↗

PubMed1994

Long-term outcome after intravenous magnesium sulphate in suspected acute myocardial infarction: the second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2)

The second Leicester Intravenous Magnesium Intervention Trial (LIMIT-2) examined the effect of an intravenous regimen of magnesium sulphate in 2316 patients with suspected acute myocardial infarction. Treatment, according to a double-blind randomised protocol, was started with a loading injection, before any thrombolytic therapy, and continued with a maintenance infusion for a further 24 h. Cause-specific mortality of randomised patients has now been examined over 1.0-5.5 (mean 2.7) years of follow-up. Mortality rate from ischaemic heart disease was reduced by 21% (95% CI 5-35%, p = 0.01) and all-cause mortality rate reduced by 16% (2-29%, p = 0.03) in magnesium-treated patients. Magnesium protects the contractile function of the myocardium from reperfusion injury ("stunning") in experimental models; this observation accords with the 25% (7-39%, p = 0.009) reduction in early left ventricular failure in the magnesium group of LIMIT-2. For such protection to occur, magnesium must be raised by the time of reperfusion since the injury is immediate. In the clinical context the timing of magnesium treatment in relation to thrombolytic therapy or spontaneous reperfusion is likely to be critical. The early benefits of this simple and safe intervention are reflected in improved long-term survival.

Double-Blind Method↗

PubMed2004

Magnesium-dependent ATPase activity and cooperativity of magnesium chelatase from Synechocystis sp. PCC6803.

The first committed step in chlorophyll biosynthesis is catalyzed by magnesium chelatase, a complex enzyme with at least three substrates, cooperative Mg(2+) activation, and free energy coupling between ATP hydrolysis and metal-ion chelation. A detailed functional study of the behavior of the intact magnesium chelatase has been performed, including characterization of magnesium cooperativity and the stoichiometry of ATP consumption in relation to the magnesium porphyrin produced. It is demonstrated that, in vitro, this catalyzed reaction requires hydrolysis of approximately 15 MgATP(2-) and that the chelation partial reaction is energetically unfavorable, under our assay conditions, with a DeltaG degrees ' of 25-33 kJ mol(-1). Given the likely metabolite concentrations in vivo, this results in the chelatase reaction operating far from equilibrium. We have also determined the steady-state kinetic behavior of the intact enzyme and have compared the kinetic parameters obtained with those observed for the partial reactions of individual subunits. K(DIX) (where D(IX) represents deuteroporphyrin IX) is estimated to be 3.20 microm, and K(MgATP)(2-) is 0.45 mm. k(cat) for chelation is estimated to be 0.8 min(-1), suggesting that the ATP hydrolysis catalyzed by the isolated ChlI subunit is substantially slower in the intact chelatase. The magnesium-rich form of the chelatase is a more effective catalyst of the chelation reaction; magnesium activation of the chelatase increases V, as well as the specificity constant for the reaction of MgATP(2-) and D(IX), possibly as a result of a magnesium-triggered conformational change.

Adenosine Triphosphate↗