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Outcome-based justification for implementing new point-of-care tests: there is no difference between magnesium replacement based on ionized magnesium and total magnesium as a predictor of development of arrhythmias in the postoperative cardiac surgical patient.

OBJECTIVE: To determine whether introducing a new laboratory test, ionized magnesium (iMg++), would affect outcome, where outcome was defined as the rate of arrhythmias in a population of postoperative cardiopulmonary bypass (CPB) patients. DESIGN: A prospective randomized trial. SETTING: Cardiothoracic surgical intensive care unit of a university hospital. PATIENTS: One hundred fifty consecutive post-CPB patients with randomized to two groups, one of which received routine reporting of iMg++ levels on all postoperative electrolyte requests while the other had access to total magnesium (tMg++) levels on demand and no access to iMg++ levels. Groups were compared for rate of arrhythmias, total amount of magnesium repleted, and demographics. MEASUREMENTS AND MAIN RESULTS: Eighty-five patients were randomized to the tMg++ group and 65 to the iMg++ group. The two groups did not differ in the rate of arrhythmias (chi-square test): 13/85 (15%) of the tMg++ patients and 12/65 (18%) of the iMg++ patients developed an arrhythmia. The groups also did not differ in the amount of magnesium sulfate (MgSO4) administered (2 tailed t-test): tMg++ patients received 1.5 +/- 0.15 (SEM) gm of MgSO4, whereas iMg++ patients received 1.3 +/- 0.15 gm. CONCLUSION: The study does not support the hypothesis that magnesium repletion titrated to iMg++ reduces arrhythmia development in post-CPB patients. The lack of a difference in the amount of magnesium replacement between the two groups suggests that tMg++ level is a reasonable indicator of iMg++ level. Routine measurement of iMg++ does not, therefore, appear to have advantages over tMg++ in the postoperative management of CPB patients.

Aged↗
PubMed1995

Editorial policy of Magnesium Research: general considerations on the quality criteria for biomedical papers and some complementary guidelines for the contributors of Magnesium Research. Society for the Development on Magnesium Research.

The quality criteria of biomedical journals--and of 'Magnesium Research' as such--are being given a new insight. This has practical implications for the contributors and the editors. General considerations on the patterns of evaluation of scientific papers highlight five types of errors, that may be incurred in submitted manuscripts. 1. The information conveyed may remain ambiguous: for example, lack of discrimination between acute and chronic patterns, or confusion between the clinical and toxicological consequences of pharmacological and physiological studies: for example it is a real scientific fraud to identify the absent toxic effects of physiological magnesium supplementation with those of high pharmacological magnesium doses ... which in fact may induce toxicity. There should be no confusion between in vitro and in vivo data, with a good understanding of the systemic neuroendocrine metabolic and renal regulations and of the multiple local targets concerned. It is always important to discriminate between the two types of deficit: deficiency due to insufficient intake which merely requires oral physiological supplements and depletion related to a dysregulation which requires more or less specific correction of its causal dysregulation. 2. Insufficient information retrieval, frequently with consultation of one data-base only. Because of indexing omissions and word usage idiosyncrasies, no literature search can retrieve all papers. Monographs and books of proceedings are rarely mentioned in databases and therefore escape consultation. It is obvious, besides, that some of the quoted references have sometimes not been read, but only the title (and in the best cases also the abstract), occasionally with the remaining misprints. A good specific and general knowledge of the background of the study is necessary. 3. Basic methodological errors. Coexistence does not mean causality. Analogous patterns do not demonstrate an identical aetiopathogenesis. The complexity of biology must not be disregarded just because the present trend focuses on one aspect of knowledge at the expense of many others. 4. Thought processes must be unbiased. Citation of supportive papers to the prejudice of unsupportive papers constitutes a real ethical fraud. It seems also very important to submit for publication papers with negative results as well as ones with positive results. In studies on pharmacological indications for magnesium, choice of the magnesium salt used ought to be justified and the efficiency must be evaluated vs reference treatment. 5. Observance of the formal regulations is frequently neglected, in the presentation of manuscripts particularly. Some guidelines should therefore be added to the directions to contributors. Before establishing valuable protocols and in order to write up well structured introductions, discussions and conclusions, the authors should have a comprehensive view of their subjects, that is to say an overall knowledge of the previous general and specific publications related to the topic which must be read. Title, conclusions and abstract ought to be taken into account in the discussion. References should be duly consulted or mentioned as 'cited in'. There should be strict observance of the presentation of the manuscripts according to the directions to contributors. Studies resulting in negative results should not be disregarded. Reciprocally, the editorial policy requires that editors and referees ought to be strict as regards the quality criteria. Although editors and peer reviewers are in no position to detect basic fraud they can, however, highlight errors, whether due to simple oversight or to more subtle ethical or scientific pseudo-frauds. Both conclusive and inconcern papers may deserve publication: positive and negative results equally concern public health. To conclude, the editorial board must be ready to reject dubious manuscripts but must at the same time keep their minds open to consider in a positive l

Animals↗
PubMed1990

Intracellular free magnesium in frog skeletal muscle studied with a new type of magnesium-selective microelectrode: interactions between magnesium and sodium in the regulation of [Mg]i.

The application of a new type of intracellular magnesium-selective microelectrode based on the neutral carrier ETH5214 to measure intracellular free magnesium ([Mg]i) in frog skeletal muscle fibers is reported. At room temperature (18-20 degrees C) the average values for [Mg]i was 0.93 mmol/l (pMgi = 3.03 +/- 0.42, SD; n = 38 experiments). The regulation of [Mg]i was studied by measuring [Mg]i and [Na]i with ion-selective microelectrodes during alterations of the membrane potential and the transmembrane sodium and magnesium gradients. Depolarization by increasing external [K] from 2.5 mmol/l to 12.5 mmol/l did not significantly influence [Mg]i. Increasing extracellular [Mg] from 1 mmol/l to 10 and 20 mmol/l caused a concentration-dependent rise in [Mg]i and a decrease in [Na]i, whereas removal of external magnesium did not affect [Mg]i. Removal of external [Na] caused an increase in [Mg]i and a decrease of [Na]i. The results show that [Mg]i in frog skeletal muscle is not in thermodynamic equilibrium and suggest that a Na/Mg exchange mechanism may be involved in maintaining low levels of [Mg]i.

Animals↗
PubMed1998

[Magnesium and calcium changes in serum and atrial muscle caused by open heart surgery and the effect of preoperative oral magnesium administration].

The study was undertaken to compare magnesium and calcium serum concentration levels and magnesium and calcium atrial muscle content of between the non-magnesium group (20 patients) and the magnesium group (11 patients) in the perioperative period of open heart surgery. In addition, the incidence of arrhythmias was compared between the two groups. Late ventricular potentials and postoperative ventricular arrhythmias were evaluated in both groups. The patients of the magnesium group were administered a daily oral intake of 3.0 g of magnesium oxide for ten days before operation. In both groups, serum concentration of magnesium decreased abruptly due to hemodilution after the operation and began increasing gradually from 24 hours after the operation. However, in the non-magnesium group the concentration decreased below the normal range in the 24 hour period after the operation and elevated to above the preoperative value from the third to fifth postoperative days. In the magnesium group serum concentration of magnesium was higher during the 24 hours after the operation and lower from the third to fifth postoperative days than the non-magnesium group. Thus, the fluctuation was smaller in the magnesium group than the non-magnesium group. Serum concentration of calcium also decreased abruptly after the operation and gradually increased in the postoperative days in both groups. However, the level was always higher in the magnesium group than the non-magnesium group. The concentration ratio of serum calcium to magnesium was relatively unchanged postoperatively in the magnesium group, whereas it decreased significantly from the second to seventh postoperative days in the non-magnesium group. Magnesium and calcium contents in the atrial muscle were measured before and after cardiopulmonary bypass. Before bypass, magnesium and calcium contents were higher in the magnesium group than the non-magnesium group. However, in the non-magnesium group the calcium content increased significantly after bypass compared to pre-bypass levels, whereas it was unchanged in the magnesium group. Ventricular arrhythmias severer than grade 3 were found in 4 cases in the non-magnesium group. On the other hand, no ventricular arrhythmias severer than grade 3 were found in the magnesium group. As to the incidence of supraventricular arrhythmias, no difference was demonstrated between both groups. The appearance of late ventricular potentials on signal averaged electrocardiograms was found variable and often transient, and no association was found between the appearance of late ventricular potentials and the incidence of ventricular arrhythmias. Smaller fluctuations of magnesium and calcium concentrations in serum as well as in the atrial muscle were observed in the postoperative days in the magnesium group. Magnesium and calcium ratio also showed smaller fluctuations in the postoperative days in the magnesium group. In conclusion, these factors, along with suppression of calcium influx in the cardiac muscle, appeared to serve to reduce the incidence of ventricular arrhythmias in the magnesium group.

Administration, Oral↗
PubMed1997

Functional magnesium deficiency in critically ill patients identified using a magnesium-loading test.

OBJECTIVE: To determine the feasibility of the magnesium-loading test in the critically ill and to validate serum ionized magnesium assay using the magnesium-loading test as a reference in this same patient population. DESIGN: Double-blind, randomized, controlled clinical investigation. SETTING: Tertiary level intensive care unit. PATIENTS: Forty-four consecutive critically ill patients without evidence of renal insufficiency. INTERVENTION: Patients were randomly allocated to receive 30 mmol (7.5 g) of magnesium sulfate daily for 3 days, or an equivalent amount of normal saline. MEASUREMENTS AND MAIN RESULTS: We recorded baseline characteristics, and serial serum biochemical measurements included creatinine, glucose, sodium, potassium, phosphate, total calcium, ionized calcium, total magnesium, and ionized magnesium. Serum assays were accompanied by 24-hr urine collections of creatinine and magnesium over the 3-day period. Baseline characteristics were comparable in both groups. In patients receiving magnesium, serum ionized magnesium and total magnesium concentrations were increased by 43% (p = .0001) and 59% (p = .0002), respectively, on day 1 as compared with the control group. Magnesium excretion in the control group averaged 4.8 +/- 2.3 mmol/day during the 3-day study period, while the magnesium excretion in the magnesium-loaded group was significantly increased to 22.7 +/- 10.9 mmol/day (p < .0001). Following day 1 magnesium loading, patients who excreted < 70% of the total magnesium (30 mmol infused magnesium plus 4.8 mmol basal excretion) were termed as functionally magnesium-deficient retainers (n = 12), and patients who excreted > 70% of the total magnesium were termed as nonretainers (n = 7). In addition, magnesium retainers on day 2 (nine of ten patients) and day 3 (five of six patients) excreted > 70% of the total magnesium, indicating a replenishment of body magnesium stores. In contrast, nonretainers on day 2 (four of five patients), and day 3 (four of four patients) continued to excrete excess amounts of magnesium. In the retainer group, only two patients had a low serum ionized magnesium concentration, while two other patients had low total serum magnesium values. In addition, magnesium retention was associated with low ionized calcium and high phosphate values. CONCLUSIONS: The magnesium-loading test is feasible and appears to be valid based on its performance during the 3-day evaluation. Using the magnesium-loading test as a reference, serum ionized magnesium appears to be an insensitive biochemical marker of functional hypomagnesemia. Larger cohort studies using the magnesium-loading test will help establish the true prevalence of magnesium deficiency and its associated risk factors in critically ill patients.

APACHE↗
PubMed1992

Brain and CSF magnesium concentrations during magnesium deficit in animals and humans: neurological symptoms.

Magnesium is an essential cofactor for many enzymatic reactions, especially those involved in energy metabolism. Deficits of magnesium are prevalent due to inadequate intake or malabsorption and due to the renal loss of magnesium that occurs in certain disease states (alcoholism, diabetes) and with drug therapy (diuretics, aminoglycosides, cisplatin, digoxin, cyclosporin, amphotericin B). Protracted deficits of magnesium in humans and animals result in neurological disturbances, including hyperexcitability, convulsions and various psychiatric symptoms ranging from apathy to psychosis, some of which can be reversed with magnesium supplementation, others requiring correction of the dysregulation mechanism. Although the role of magnesium in neuronal function is not completely understood, a lowering of CSF or brain magnesium can induce epileptiform activity and there is an association between decreased CSF magnesium and the development of seizures. CSF concentrations of magnesium are normally higher than magnesium plasma ultrafiltrate (diffusible) concentrations due to the active transport of magnesium across the blood-brain barrier. Under conditions of magnesium deficiency, CSF concentrations decline, although this decline lags behind and is less pronounced than the changes observed in plasma magnesium concentrations. Decreases in CSF magnesium concentrations correlate with the alterations observed in extracellular brain magnesium concentrations in animals following the dietary deprivation of magnesium. CSF magnesium concentrations can readily be repleted following magnesium supplementation, although high dose magnesium therapy, such as that used in the treatment of convulsions in eclampsia, will only increase CSF magnesium concentrations to a very limited degree (approximately 11-18 per cent) above physiological concentrations. Greater increases in CSF magnesium may occur in neonates since neonatal swine, following treatment with magnesium, have CSF magnesium concentrations that are similar to their plasma concentrations. There has been a recent resurgence of interest in magnesium deficiency and its neurological consequences due to the finding that magnesium, at physiological concentrations, blocks N-methyl-D-aspartate (NMDA) receptors in neurones. NMDA receptors are normally activated by glutamate and/or aspartate which represent the principal neurotransmitters for excitatory synaptic transmission in vertebrate CNS. Magnesium deficiency produces epileptiform activity in the CNS which can be blocked by NMDA receptor antagonists. Other mechanisms, including alterations in Na+/K(+)-ATPase activity, cAMP/cGMP concentrations and calcium currents in pre- and postsynaptic membranes, may also be at least partially responsible for the neuronal effects associated with low brain magnesium. Further studies are necessary to increase our understanding of the neurological implications of magnesium deficit in the central nervous system.

Animals↗
PubMed1995

Progressive magnesium deficiency increases mortality from endotoxin challenge: protective effects of acute magnesium replacement therapy.

OBJECTIVES: To study the effects of endotoxin on magnesium homeostasis; to determine if progressive magnesium deficiency alters outcome from endotoxin challenge; and to evaluate the efficacy of magnesium therapy in reducing endotoxin-induced mortality. DESIGN: Prospective, placebo-controlled, randomized, multiexperiment studies. SETTING: Research laboratory of a university hospital. SUBJECTS: Male Sprague Dawley rats (n = 299). INTERVENTIONS: Experiment 1 was designed to test if endotoxin alters magnesium homeostasis. Circulating total and ionized magnesium (estimated by ultrafilterable values) concentrations were determined in blood samples collected from animals after the randomized administration of placebo or 0.3, 3.0, or 30 mg/kg of endotoxin. A baseline blood sample was collected and then a second blood sample was obtained at 5, 15, 30, 60, 120, or 180 mins after endotoxin or placebo administration. In experiment 2, animals were randomized to receive magnesium-sufficient diets or magnesium-deficient diets for 6 wks. After 6 wks, the effects of the randomized administration of 3.0 mg/kg endotoxin or placebo were evaluated on mortality and analyte values (pH and blood gases, sodium, potassium, chloride, glucose, ionized calcium, hematocrit, total and ultrafilterable magnesium concentrations) in the three study groups (magnesium-sufficient, 3-wk magnesium-deficient, or 6-wk magnesium-deficient). In experiment 3, magnesium-deficient animals were randomized to receive 50 mmol/kg magnesium chloride or placebo, before or after the administration of 3.0 mg/kg of endotoxin. Baseline and 24-hr analyte determinations were performed and outcome was analyzed. MEASUREMENTS AND MAIN RESULTS: Experiment 1: Significant increases (p < .05) in circulating total magnesium concentrations were found in animals that received 30 mg/kg of endotoxin, at 120 mins (0.79 +/- 0.10 vs. 0.60 +/- 0.05 mmol/L), and 180 mins (0.74 +/- 0.04 vs. 0.56 +/- 0.04 mmol/L) compared with baseline values. Similarly, significant increases (p < .05) in ionized magnesium concentrations were observed 120 and 180 mins after 3.0 and 30 mg/kg of endotoxin compared with baseline values. Experiment 2: Magnesium deficiency was strongly (p < .02) associated with increased mortality from endotoxin challenge. Endotoxin administration (3.0 mg/kg) was lethal in 10 (43%) of 23 magnesium-sufficient animals, 15 (65%) of 23 3-wk magnesium-deficient animals, and 20 (83%) of 24 6-wk magnesium-deficient animals. Experiment 3: In magnesium-deficient animals, rats treated with magnesium replacement therapy had significantly increased survival from endotoxin administration (15 [52%] of 29 vs. five [17%] of 29, p < .01) compared with placebo-treated animals. CONCLUSIONS: a) Endotoxin challenge causes significant increases in circulating total and ionized magnesium concentrations. b) Progressive magnesium deficiency is strongly associated with increased lethality, and magnesium replacement therapy provides significant protection from endotoxin challenge. c) These experimental results support the concept that cellular injury is probably associated with increases in circulating magnesium concentrations. Furthermore, these experimental findings suggest that magnesium deficiency predisposes to worse outcome from endotoxin challenge, and that replacement therapy in the setting of magnesium deficiency may be warranted, especially in critically ill subjects.

Animals↗
PubMed1999

Magnesium, citrate, magnesium citrate and magnesium-alkali citrate as modulators of calcium oxalate crystallization in urine: observations in patients with recurrent idiopathic calcium urolithiasis.

The effects of magnesium (Mg) and citrate on the metastable limit of calcium oxalate (CaOx) solubility (synonym: tolerable oxalate TO) were examined in artificial urine and in postprandial urine of male patients with idiopathic calcium urolithiasis (ICU). In artificial urine increasing pH, Mg and citrate elevate TO, decrease CaOx supersaturation only marginally, but elevate considerably free citrate; the effect of Mg alone was small in comparison with citrate alone, and the effects of both substances appeared additive. In ICU patients, matched for sex, age and CaOx supersaturation to non-stone-forming controls, TO was decreased (mean values 0.33 vs. 0.52 mM/l in controls, P < 0.05). Additional significant (P < 0.05) differences were found between ICU and controls: the former exhibited increased CaOx crystal growth, decreased crystal agglomeration time, a more acidic urinary pH, increased concentrations of free calcium and free Mg, and decreased free oxalate and free citrate. After ingestion of a urine-acidifying test meal, or this meal supplemented with either neutral Mg citrate or Mg-alkali citrate, by three groups of male ICU patients, matched for age and CaOx supersaturation, only the last-named preparation evoked an increase in TO and a decrease in crystal diameter, while the normally occurring pH decline from fasting urine was virtually abolished, and the ratios urinary Mg/citrate and calcium/citrate tended towards low values. In contrast, Mg citrate increased crystal agglomeration time, while changes in the other parameters were only insignificant. The crystals formed in urine were CaOx di- and monohydrate (by electron microscopy), and energy dispersive X-ray analysis showed calcium peaks exclusively. However, chemical analysis of crystals verified the presence not only of oxalate and calcium, but also of Mg, phosphate, citrate, and urate; moreover, these crystal constituents seemed to be influenced by Mg citrate and Mg-alkali citrate in different ways. It was concluded that (1) Mg and citrate are effectors of TO in artificial and natural urine; (2) in ICU, low TO and other disturbed CaOx crystallization parameters appear related to the prevailing low urinary pH and low free citrate; (3) Mg-alkali citrate inhibits CaOx crystallization, probably via actions of the citrate, but not the Mg. Because of the eminent role of Mg in human health and ICU, further studies on crystallization after oral intake of Mg in the form of citrate are warranted.

Calcium Oxalate↗
PubMed1998

Bioavailability of magnesium contained in roasted and ground soybean (kinako) as evaluated by serum and bone magnesium contents, kidney calcification, and magnesium absorption.

The bioavailability of roasted and ground soybean (kinako) magnesium (Mg) in Fischer 344 strain male rats with respect to serum Mg level, bone Mg contents, kidney calcification, and Mg absorption was evaluated. Four-week-old male rats were divided into four groups of six rats each. The four groups were the control (20SC), Mg-deficient diet (1/3 Mg20SC), 20SCK diet, and 20SCDK diet. The 20SCK and 20SCDK diets were prepared to contain amounts of Mg equal to that in the 20SC diet with kinako or defatted kinako as the Mg source, respectively. After a 4-week experimental period, rats were decapitated and blood serum, right femur, and right kidney were collected, and Mg, calcium (Ca), and phosphorus (P) concentration in those tissues were determined. The Mg balance was also investigated. The serum Mg concentration in the 1/3 Mg20SC group was half the level in the 20SC group, and the serum Ca concentration was higher than in the 20SC group, indicating apparent hypercalcemia. Serum Mg and Ca concentrations in the 20SCK and 20SCDK groups did not significantly differ from those in the 20SC group. Femur Mg concentration in the 1/3 Mg20SC group was lower than in the 20SC group. Femur Mg concentrations in the 20SCK and 20SCDK groups were lower than in the 20SC group, but significantly higher than in the 1/3 Mg20SC group. The kidney Ca concentrations in the 20SCK and 20SCDK groups were significantly higher than those in the 20SC and 1/3 Mg20SC groups, and there was also kidney calcification. These results indicated that kinako and defatted kinako Mg were used effectively as a serum and femur Mg source, but that kinako and defatted kinako carry a risk of kidney calcification when used as the only Mg source.

Absorption↗
PubMed2000

The impact of diets with different magnesium contents on magnesium and calcium in serum and tissues of the rat.

The impact of three different magnesium diets (70, 1,000 and 9,000 ppm) on total, ionized and bound magnesium as well as ionized calcium in serum and total calcium and magnesium in femoral bone, skeletal muscle, heart and liver of male Sprague-Dawley rats was investigated. The percentage of ionized serum magnesium was unproportionally high in rats fed a low magnesium (70 ppm) diet. Femoral magnesium was correlated with ionized and total serum magnesium. In contrast, there was generally no correlation between total serum magnesium and the magnesium fractions in skeletal muscle, heart and liver. In rats fed the magnesium deficient diet, total cardiac concentration of magnesium was even significantly increased along with total calcium content, while there were no effects on total muscle and liver magnesium. Within the single groups, ionized serum calcium was never proportional to dietary magnesium, but in all three magnesium diet groups together, it was inversely correlated with dietary magnesium. Moreover, ionized serum calcium was inversely correlated with both ionized and total serum magnesium. In all 3 groups together, the concentrations of total calcium and magnesium in heart and skeletal muscle were correlated, within the single groups correlation existed only in the 1000 ppm group. Magnesium influx via calcium channels during low magnesium intake has been seen in non cardiac tissues [35,36], but nothing similar is known about non selective channels for divalent cations in the heart [33]. Thus, magnesium uptake by cardiac cells along with calcium seems to be possible, especially at low intracellular magnesium concentrations, but is still poorly investigated. We suggest that the calcium-antagonistic effect of magnesium is related to the turnover rate of magnesium rather than to its tissue concentrations.

Animals↗
PubMed1987

Magnesium reabsorption in the juxtamedullary loop of Henle: effect of magnesium deprivation.

To determine the contribution of the juxtamedullary loop of Henle to magnesium reabsorption during magnesium deficiency, we performed two-phase micropuncture studies of end-descending limbs in a group of magnesium-deficient rats (n = 7) and in a pair-fed control group (n = 8) given MgCl2 in their drinking water. In the magnesium-deficient rats, daily excretion of magnesium fell to very low values (1.2 +/- 0.2 vs. 52 +/- 12 microM.day-1.100 g body weight-1, p less than 0.05). Plasma magnesium concentration and fractional magnesium excretion during the control phase were nearly 52 and 27%, respectively, of the values observed in pair-fed controls. Fractional magnesium delivery to the end-descending limb did not differ significantly between the two groups. During the acute magnesium repletion phase, fractional magnesium excretion and fractional magnesium delivery to the end-descending limb increased by a similar value in the two groups of rats, despite a lower filtered load of magnesium in the magnesium-deficient group. Absolute magnesium reabsorption upstream to the end-descending limb was lower in the magnesium-deficient rats but was otherwise tightly coupled to the filtered load of magnesium (Y = 0.91 + 0.37 x, r = 0.82, p less than 0.05). Similar observations were made with regards to whole kidney magnesium reabsorption. Our results suggest that, in young magnesium-deficient rats, magnesium reabsorption is tightly coupled to the filtered load of magnesium both in segments upstream to the juxtamedullary end-descending limb and in the whole kidney, and that a reabsorptive defect for magnesium is not evident in this setting.

Animals↗
PubMed2005

Do intracellular, extracellular or urinary magnesium concentrations predict renal retention of magnesium in critically ill patients?

BACKGROUND AND OBJECTIVE: Magnesium disorders are common in hospitalized patients. In patients with low or normal magnesium, the intravenous magnesium loading test has been demonstrated to be a sensitive test to assess magnesium deficiency in critically ill patients. However, it is more time consuming and more difficult than the measurement of intracellular or extracellular magnesium concentrations. This study evaluated whether erythrocyte, plasma and urinary magnesium concentrations predict renal magnesium retention measured by th magnesium loading test. METHODS: One-hundred-and-three intensive care patients (36 females, 67 males) in a tertiary care centre and 41 healthy subjects (13 females, 28 males) took part in this prospective study. Intracellular, total plasma, ionize extracellular and urinary magnesium concentrations were measured and also magnesium retention by intravenous magnesium loading test. RESULTS: Total plasma magnesium concentration was poorly correlated with magnesium retention (r = 0.36 r2 = 0.13) and was the only parameter that significantly predicted magnesium retention in intensive care patients (P < 0.01). However, only 10% of the magnesium retention data were linked to the total plasma magnesium concentration. CONCLUSIONS: Total plasma magnesium concentration predicts magnesium retention in critically ill intensive care patients but not intracellular and urinary magnesium concentrations. Only a small proportion of the magnesium retention was due to the total plasma magnesium concentration.

Critical Care↗
PubMed1998

Short time effect of Chemiron (a combination iron preparation), single iron, and different magnesium salts on plasma. Magnesium concentration during early pregnancy in Nigerian women. A preliminary report.

Maternal magnesium requirements increase during pregnancy because of the synthesis of new tissue--both fetal and maternal. Magnesium takes part in almost 300 enzymatic reactions in the human body and regulates membrane permeability and protein bio-synthesis by promoting initiation and dissociation factors. The absorption velocity of magnesium differs from one tissue to another in animal experiments. It is highest in the liver, kidney, heart and is low in skeletal muscle, the brain and erythrocytes. It obeys and follows the Michaelis-Menten Kinetic law. 15 mmol of magnesium is consumed daily depending on the types of food takenin. The main sources of magnesium are vegetables and meats. Many Nigerian women are not able to afford enough of these. The amount of magnesium reabsorbed depends on the magnesium intake and not on magnesium needed which is about 10-40% of the intake. In this study, we examined the short-term effect of magnesium asphat HCL (614.18 mgMG), magnesium diasporal (magnesium citrate 610 mg + magnesium laevalitat 30 mg = 100 mg magnesium = 8.2 mval), ferrous gluconate (300 mg) plus folic acid and chemiron, a new combination hematinic agent (ferrous fumarate 300 mg, folic acid 5 mg, vitamin B12 10 mg, vitamin C 25 mg, magnesium sulfate 0.3 mg and zinc sulfate 0.3 mg) on plasma magnesium concentration during early pregnancy in Nigerian women. Significant increases of plasma magnesium concentrations were found in these groups (magnesium asphat HCL, 0.83 +/- 0.12 to 0.96 +/- 0.14 mmol/l, magnesium diasporal 0.843 +/- 0.14 to 0.891 +/- 0.14 mmol/l and chemiron 0.848 +/- to 0.866 +/- 0.16 mmol/l after five days. The ferrous gluconate and folic acid treated group showed no significant changes. This study shows that a chemiron supplement leads to increased magnesium plasma levels whereas ferrous gluconate and folic acid do not. These results suggest that the low level of magnesium is a normal physiological adjustment of pregnancy and that iron supplementation does not influence this unless magnesium salt is given.

Adult↗
PubMed2002

Exchangeable magnesium pool masses in healthy women: effects of magnesium supplementation.

BACKGROUND: Studying magnesium pools in the body with use of stable isotopes may be helpful for evaluating magnesium status. Data on the evaluation of magnesium pools in humans are scarce. OBJECTIVE: We undertook this study to evaluate the effects of a magnesium supplementation program on the size of the exchangeable body pools of magnesium and on classic indexes of magnesium status in healthy women with normal magnesium status. DESIGN: Ten healthy women participated in a kinetic study with magnesium stable isotopes before and after 8 wk of magnesium supplementation. Each woman received 3 supplements containing 5.08 mmol (122 mg) elemental Mg/d (366 mg/d). Before and at the end of the supplementation period, each woman received an intravenous injection of 1.67 mmol (40 mg) (25)Mg, and the plasma magnesium disappearance curve was followed for the next 7 d. Two methods were used to analyze the exchangeable pools of magnesium: 1) formal multicompartmental modeling and 2) a simplified estimation of the total mass of the rapidly exchangeable magnesium pool (EMgP). RESULTS: In these healthy women, exchangeable magnesium pools represented 11-12% of total body magnesium on the basis of multicompartmental analysis. The simplified estimation of EMgP overestimated the size of the exchangeable magnesium pools by approximately 45-50%. Eight weeks of magnesium supplementation did not significantly modify the size of the exchangeable magnesium pools, whereas urinary magnesium excretion was significantly higher after 8 wk of supplementation. CONCLUSION: Women with no clinical evidence of magnesium deficiency may not respond to short-term supplementation with increases in the mass of the exchangeable magnesium body pool or in magnesium turnover rates.

Adult↗
PubMed1999

Effect of potassium magnesium citrate on thiazide-induced hypokalemia and magnesium loss.

The study was performed to ascertain the value of potassium magnesium citrate, magnesium citrate, and potassium citrate in overcoming thiazide-induced hypokalemia and magnesium loss. Sixty-two healthy subjects were first administered hydrochlorothiazide, 50 mg/d. After 3 weeks of thiazide treatment (or earlier for potassium level </=3.5 mEq/L), they were randomized to receive one of three drugs while continuing to receive thiazide: potassium magnesium citrate (49 mEq of potassium, 24.5 mEq of magnesium), magnesium citrate (24.5 mEq/d of magnesium), or potassium citrate (49 mEq/d of potassium). Outcome measures were changes in serum potassium and magnesium levels and urinary potassium, magnesium, pH, and citrate values. All three drugs increased serum potassium concentration compared with that resulting from thiazide alone. Potassium magnesium citrate increased serum potassium levels from 3.3 +/- 0.2 to 3.8 +/- 0.3 mEq/L (P < 0.001), potassium citrate increased serum potassium levels from 3.4 +/- 0.4 to 3.9 +/-0.3 mEq/L (P < 0.001), and magnesium citrate from 3.4 +/- 0.4 to 3.7 +/- 0.3 mEq/L (P < 0.001). Potassium magnesium citrate led to a significant increase in urinary magnesium levels by the third week of supplementation (from 120 +/- 34 to 149 +/- 58 mg/d; P < 0.01) and produced a small but significant increase in serum magnesium level. Magnesium citrate significantly increased 24-hour urinary magnesium after the first week of supplementation and maintained this increase throughout the study. Potassium magnesium citrate and potassium citrate, but not magnesium citrate, significantly increased urinary pH and citrate values. Potassium magnesium citrate not only corrects thiazide-induced hypokalemia, but also may avert magnesium loss while providing an alkali load.

Adult↗
PubMed1985

Effect of magnesium loading on magnesium delivery to the juxtamedullary end-descending limb.

Previous micropuncture and microperfusion studies in acutely hypermagnesemic rats have yielded conflicting results with respect to magnesium transport in Henle's loop. The following experiments were performed to reexamine, by micropuncture of papillary end-descending limb, whether magnesium undergoes intratubular secretion in magnesium-loaded rats. Group 1 animals served as normal controls; group 2 animals received an acute intravenous magnesium load; group 3 animals were orally magnesium loaded for 3 wk before receiving an acute intravenous magnesium load during micropuncture; group 4 animals were acutely thyroparathyroidectomized and water loaded before receiving an acute magnesium load. Fractional magnesium delivery to the end-descending limb did not differ from the corresponding value observed in the superficial proximal tubule in normal animals (67 +/- 5.3 vs. 76 +/- 7.6%). Acute magnesium loading raised plasma magnesium concentration and fractional magnesium excretion more than twofold but did not change fractional magnesium delivery to the end-descending limb or superficial nephron significantly from control values (75 and 73%). Chronic oral magnesium loading raised daily urinary magnesium excretion threefold (183 vs. 53 mumol X day-1 X 100 g body wt-1, P less than 0.05), but acute magnesium loading in this group did not significantly alter fractional delivery to the end-descending limb (85 +/- 10%, NS). Increasing intratubular flow rate while acutely raising plasma magnesium concentration (group 4) also did not induce intratubular magnesium secretion. The absence of significant changes in fractional magnesium delivery to the end-descending limb during magnesium loading suggests that intratubular magnesium secretion, if at all present, is very small and of questionable significance.

Animals↗
PubMed1974

Effect of age and magnesium depletion on bone magnesium pools in rats.

In vivo and in vitro studies were carried out to characterize the exchangeable bone magnesium pool and determine what effect age and magnesium depletion has on bone magnesium. A highly significant correlation was found between the size of the in vitro elutable and in vivo exchangeable bone magnesium (r=0.97). To show that the exchangeable bone magnesium was the surface-limited bone magnesium, elution studies were performed 4 h after the in vivo administration of radiomagnesium. Specific activity in the eluant was 85% of that found in the serum at time of death, suggesting that the elutable and exchangeable bone magnesium pools were largely the same pool. Bone magnesium concentration fell with increasing age. The entire fall in bone magnesium was a result of a decrease in the surface-limited fraction. Since bone crystals have been shown to enlarge with aging with resulting contraction of the surface area, this would be the most apparent explanation for this finding. During magnesium depletion, magnesium concentration in both the exchangeable and nonexchangeable pools decreased. The fractional change in the exchangeable pool was much larger than the change in total or nonexchangeable bone magnesium, suggesting that the surface-limited magnesium pool is available during magnesium depletion. The change in size of the nonexchangeable bone magnesium pool appeared to be more related to the duration of magnesium depletion than the change in serum magnesium levels. The fall in magnesium concentration in this pool is probably a consequence of continuing formation of low magnesium bone during the depletion period.

Aging↗