Plasma Mg Concentrations Research Articles

Assessment of magnesium intake according to requirement in dairy cows.

To date, no specific hormonal regulation system has been identified for homoeostatic control of the essential mineral Mg. In cattle, the maintenance of physiological plasma Mg concentration depends on gastrointestinal absorption, primarily from the rumen, which serves as a pool for covering the requirement. Whereas a possible surplus (absorption greater than requirement) is rapidly excreted by the kidneys, a shortage (absorption lower than requirement) cannot be compensated for by mobilization from the large Mg pool in bones or soft tissue, so that the maintenance of the necessary physiological Mg concentration in plasma relies on continuous and sufficient absorption. Our knowledge concerning the site and mechanisms of Mg absorption has improved during the last few decades, and meta-analyses of the absorption of Mg in dairy cows have shown that the K content has a pronounced negative effect on Mg digestibility. The current recommendations of Mg intake propose a constant percentage of Mg and emphasize the depressive effect of high potassium (K) intake on Mg absorption. The current knowledge about the antagonism between K intake and Mg absorption allows a more flexible solution which includes the K content of the diet. An assessment of Mg intake is proposed that incorporates the improved knowledge of Mg absorption, metabolism and requirement. Within this framework, an equation is derived that allows a prediction of the amount of Mg required to compensate for dietary K content, the goal being to avoid both possible undernutrition or an unnecessary surplus of dietary Mg.

Calcium and magnesium status of pregnant ewes grazing southern Australian pastures

During pregnancy, ewes graze pastures that may be marginal in calcium (Ca) and magnesium (Mg), and may also be low in sodium (Na) and high in potassium (K), with a high dietary cation–anion difference. Such pastures may increase susceptibility to hypocalcaemia and hypomagnesaemia, leading to lamb losses. Clinical hypocalcaemia and hypomagnesaemia do occur in Australian sheep; however, it is unknown whether subclinical forms of these disorders compromise ewe or lamb health and survival. The present study monitored the Ca and Mg status of ewes in late pregnancy, so as to evaluate the risk of subclinical mineral disorders in ewes grazing typical southern Australian pastures. Calcium and Mg concentrations in pasture, ewe plasma and urine were monitored in 15 flocks in southern Australia. Mineral concentrations in pasture did not indicate a widespread risk of Ca or Mg deficiency; however, urinary pH and Ca and Mg concentrations in the plasma and urine of the pregnant ewes were not entirely consistent with the expectations from pasture analysis. Urine pH was above 7 on all properties and 87.5% of properties had a mean Ca in urine below the adequate concentration of 1 µmol/mosmol. The mean plasma Ca concentration was below adequate (<90 mg/L) on only one farm but five farms had more than 20% of ewes with below adequate Ca in plasma. In addition, although average farm concentrations of plasma and urine Mg indicated adequate Mg status of the ewes (>18 mg/L), more than 20% of ewes on six farms had below adequate concentrations of plasma Mg. Only one-third of the farms had 100% of ewes measured with adequate concentrations of plasma Ca (4/15) or Mg (5/15). The mineral concentrations in pre-lambing blood and urine samples suggested that a significant number of animals grazing southern Australian pastures during winter may be at risk of subclinical hypocalcaemia and hypomagnesaemia.

Carryover effects of potassium supplementation on calcium homeostasis in dairy cows at parturition

The purpose of this study was to test whether supplementation with K improves bone mineral density (BMD) in older cows so that by parturition their bone is better able to mobilize Ca. Twenty-four Holstein Friesian cows (6 mo pregnant, lactating, and in their third or later lactation) were allocated to 2 equal groups and individually fed twice daily a total diet comprising low K oaten hay plus a pelleted concentrate fortified with or without K2CO3 to achieve 3.12% K/kg of DM in the total diet of the K-supplemented (KS) cows compared with 1.50% K/kg of DM for the control cows. The cows were fed their respective diets from the beginning of their sixth month of pregnancy until 2 wk before the expected date of parturition. The strategy was to use K to stimulate a mild increase in extracellular pH to potentially improve BMD well before parturition, when high K contents in the diet are considered safe, but cease supplementing in the few weeks prepartum, when high intakes of K are known to be problematic. The expectation was that the effect of the denser bone would carry through to benefit the cow's plasma Ca, P, and Mg status at parturition. Prior to the period of K supplementation, the cows were part of a commercial pasture-based herd, to which they were returned at the end of the supplementation period and treated as 1 group from at least 11 d prepartum until the end of the study at d 42 of the next lactation. Supplementation with K successfully induced a sustained increase of urinary pH throughout late lactation and into the dry period, as expected. The KS cows consistently averaged a urine pH 0.25±0.10 U higher than the controls. However, there was no significant effect of K supplementation on BMD, bone mineral concentrations, plasma osteocalcin, urinary deoxypyridinoline:creatinine plasma Ca, or plasma P concentrations during or immediately after the cessation of supplementation, nor where there any carryover effects during parturition or by d 42 of lactation. Instead, there was an unexpected decrease in the concentration of Mg in plasma of the KS cows compared with the control cows that extended from 0.5 to 2.5 d postpartum. The timing of the decline in plasma Mg was paralleled by declines in plasma concentrations of 1,25 dihydroxy-vitamin D3 and urinary excretion of Ca and Mg, whereas urinary excretion of P increased; all changes were consistent with a hypomagnesemia that could increase the risk of hypocalcemia. These data suggest that, in addition to the well-documented negative effects of K when fed immediately at parturition, the effects of high dietary K diets can carry over for at least 11 d to trigger a mild hypomagnesemia at parturition. Because K supplementation did not improve BMD prepartum, it was not possible to conclude for or against an ability of denser bone to reduce the risk of hypocalcemia in older cows at parturition.

Magnesium concentration in plasma, leukocytes and urine of children with intermittent asthma

Background: Magnesium (Mg) is involved in numerous physiological functions, including protein folding, intracellular signalling and enzyme catalysis. It acts as a smooth muscle relaxant. We decided to test changes of total Mg concentration in plasma, leukocytes and urine of 16 healthy children and 26 patients with intermittent asthma aged 3 to 14 years. Methods: Samples were taken on the first day of bronchoobstruction and five days after the acute attack. During this period, patients were under salbutamol therapy. Results: Plasma Mg concentration in patients increased by about 40% (first day 0.58±0.05 mmol Mg/l and five days later 0.64±0.04 mmol Mg/l) compared with healthy children (0.42±0.04 mmol Mg/l). Leukocyte Mg concentrations showed significant changes. On the first day of bronchoobstruction, Mg in leukocytes significantly decreased by about 60% (1.16±0.31 mmol Mg/g protein) compared to healthy children (3.04±0.68 mmol Mg/g protein). Five days later, Mg values significantly increased (3.28±1.09 mmol Mg/g protein) and almost reached the values of the healthy group. Mg concentration in urine statistically decreased by about 30% (0.55±0.06 mmol Mg/mmol creatinine) on the first day of bronchoobstruction compared to healthy children (0.75±0.05 mmol Mg/mmol creatinine). Five days after the acute attack, Mg concentration in patients' urine (0.73±0.07 mmol Mg/mmol creatinine) was close to values of healthy children. Conclusion: The results obtained indicate that the intracellular measurement of Mg concentration is relevant for estimation of magnesium concentration in the human organism. Hence, determination of Mg concentration in lekocytes may be used in evaluation of asthmatic pathology.

Effects of virginiamycin and salinomycin on performance, digestibility of nutrients and mortality of rabbits

A total of 432 weaned Hyla 2000 rabbits was used to evaluate the effect of virginiamycin (a feed antibiotic), salinomycin (a coccidiostat) and their combination on performance, digestibility of nutrients, blood composition, slaughter parameters, incidence of coccidia and mortality. Virginiamycin and salinomycin were supplied at 30 and 20 mg/kg of a granulated feed, respectively. In a feeding trial, 100 rabbits per treatment were used. From the beginning (day 33–34 of age) to the end (day 86–87), control rabbits gained 31.4 g day −1, on an average. Daily weight gains of rabbits fed virginiamycin, salinomycin and a combination of virginiamycin and salinomycin were 33.8, 33.5 and 35.8 g day −1, respectively ( p < 0.05). The combination of feed additives decreased mortality from 12% (control) to 2% ( p < 0.001). In a digestibility trial, 32 rabbits were allotted to the same dietary treatments. Virginiamycin significantly decreased digestibility of fibre and increased that of fat. Salinomycin increased concentration of Mg in plasma. There were no important differences in other digestibility and blood variables determined. No significant effects of additives on slaughter parameters (except hindleg and perirenal fat proportions) were found. Salinomycin decreased the incidence and intensity of infection by Eimeria sp. and completely eliminated cryptosporidia.

Changes in intracellular magnesium concentrations during cisplatin chemotherapy.

Magnesium is mainly an intracellular cation, and its availability is not represented reliably by plasma levels. The effects of cisplatin on Mg concentrations in plasma (PMg) and erythrocytes (EMg) were investigated in 22 neoplastic patients. Assays were done before and 1, 2, 4 and 7 days after cisplatin administration; 10 patients were also checked following six courses of chemotherapy. PMg decreased progressively either day by day after a single dose of cisplatin (p < 0.001 on the 7th day) or month by month after cumulative doses (p < 0.05 after two courses and p < 0.001 after six). EMg decreased till the 4th day (p < 0.001), but recovered pretreatment levels on the 7th day; an actual depletion was manifested only after the third course of chemotherapy (p < 0.05) and became more marked after the 6th. These results suggest that, besides renal Mg wasting, Mg metabolism is influenced by cisplatin also at a cellular level. The cisplatin-induced injury on membrane transport systems, where Mg is abundant and plays an important stabilizing role, might induce an early shift of Mg from cells into the blood stream. When repair systems begin to act, Mg is taken up from plasma to recover the normal cellular content. The lack of an actual depletion of Mg body stores till the third course of chemotherapy possibly makes the early Mg supplementation commonly administered before or contemporaneously to cisplatin infusion unnecessary. Oral supplements between the courses might be sufficient to prevent Mg depletion without exposing the patients to the risk of hypermagnesemia in case of cisplatin-induced acute renal failure.

The role of magnesium in cardiac arrhythmias

T HE RELATIONSHIP between electrolyte deficiencies and the development and prevention of cardiac arrhythmias has been a subject of continued interest in the medical literature. Studies have suggested a correlation between certain electrolyte deficiencies, such as hypokalemia, and the occurrence of arrhythmias and sudden death.le6 Recent interest, however, has focused on magnesium (Mg) deficiency and its role in this area. Interest in Mg may be related to the recognition of the extensive role this cation plays in a multitude of human physiological processes. Mg is the second most abundant intracellular cation in the human body and is involved in over 300 different enzymatic reactions including: glucose use; the synthesis of fat, protein, and nucleic acids; the metabolism of adenosine triphosphate (ATP); muscle contraction; and some membrane transport systems. Effects of Mg on atrioventricular (AV) nodal conduction, the transmembrane potential, and arrhythmias have also been postulated.‘*7-12 Total body Mg stores approximate 1,000 mmol/L with 1% present extracellularly, 60% present in skeletal tissue, and 39% present intracellularly.’ A normal homeostatic level of Mg is maintained via a balance between gastrointestinal absorption and renal excretion. Gastrointestinal net absorption is approximately 35% to 40% of an orally administered load and occurs almost exclusively via the small intestine. Mg loss occurs primarily via renal excretion and averages only 3% to 5% of a filtered load. Over 65% of Mg reabsorption occurs in the thick ascending limb of Henle and, depending on the Mg concentration in plasma, excretion may range from 10 to 5,000 mg over a 24-hour period.274F7,97’0*‘3-15 Despite the apparent ability of the human body to maintain Mg homeostasis through intestinal and renal processes, Mg deficient states occur and are being increasingly recognized. Two studies have documented the prevalence of Mg deficiency in hospitalized patients.‘6-‘8 In one study the prevalence of hypomagnesemia was determined in 2,300 patients in a Veteran’s Administration hospital.16*” When hypomagnesemia was defined as a serum Mg concentration less than 1.25 mEq/L the prevalence of hypomagnesemia was 6.9%. In another study Wong et all8 determined serum magnesium levels in 621 samples of randomly selected hospitalized patients and found hypomagnesemia (< 1.2 mEq/ L) in 11%. The causes of hypomagnesemia are many and varied and include: nutritional causes secondary to prolonged parenteral fluid administration, starvation with metabolic acidosis, protein-calorie malnutrition, Kwashiorkor, or alcoholism; intestinal causes secondary to chronic diarrhea or a malabsorption syndrome; renal causes secondary to disease-related states such as renal tubular acidosis, the diuretic phase of acute tubular necrosis, chronic glomerulonephritis, chronic pyelonephritis, or familial and sporadic renal Mg losses; drug-related causes secondary to diuretics, antibiotic therapy including gentamicin, tobramyocin, ticarcillin, carbenicillin, or amphoteritin B, antineoplastic drugs including cisplatin and cyclosporine; endocrine and metabolic causes including primary and secondary aldosteronism, hyperthyroidism, excessive lactation, pregnancy, hypercalcemia, primary hyperparathyroidism, uncontrolled diabetes mellitus with glucosuria, and acute intermittent porphyria; and congenital causes including maternal diabetes, maternal hyperparathyroidism, maternal hypothyroidism and exchange transfusions.7’9”0~1’7’7*‘9’20 In light of the multitude of etiologies of hypomagnesemia and its prevalence in hospitalized patients, it is possible that reduced Mg often goes undetected by the unsuspecting physician. The symptoms of hypomagnesemia are as varied as its causes, yet these may often be absent or vague. 9*21 Documented manifestations include: neuromuscular symptoms including tremor, myoclonic jerks, convulsions, Chvostek sign, Trous-

Erythrocyte electrolyte abnormalities.

In contrast to lymphocytes and skeletal muscle cells, erythrocyte electrolytes may be easily determined. In this study Na, K, and Mg concentrations in plasma and erythrocytes of 100 consecutive ICU patients were compared to evaluate their potential clinical usefulness. The predictive indices of electrolyte changes in plasma vs. those in erythrocytes were low for all of the electrolytes studied. The erythrocyte Mg assessment was particularly useful for the high frequency of abnormalities observed, because it was less affected than plasma Mg by such transitory clinical states as hemodilution or lipolysis. The erythrocyte K was less frequently altered; no patient with a high K deficit was studied, excluding one patient with Crohn's disease. Finally, abnormally high erythrocyte Na levels correlated closely with some pathologic status, in particular respiratory failure.

Plasma and cerebrospinal fluid concentrations of magnesium in epileptic children

In order to discriminate between conflicting reports in the literature, plasma and cerebrospinal fluid magnesium levels from epileptic children were compared with those of control children. To exclude the possibility of methodological artifacts, two methods for Mg determination were used: atomic absorption spectrophotometry and a colorimetric procedure. By both methods a significantly decreased concentration of Mg in plasma was found in epileptics. A positive correlation of the hypomagnesemia with the severity of epilepsy was found: the more severe the epilepsy, the lower was the plasma Mg. A significant increase of Mg concentration in CSF of epileptics was found. The most likely origin of Mg in CSF in epilepsy is the CNS tissue from which Mg is released. It is suggested that these alterations of Mg concentrations in plasma and CSF originate from a functional impairment of the cell membranes which might occur in epilepsy.

Immunoreactive parathyroid hormone, calcium, and magnesium in human cerebrospinal fluid.

Parathyroid hormone (PTH) was measured radioimmunologically in simultaneous plasma and cerebrospinal fluid (CSF) samples obtained from 72 patients aged 20 to 80 years without endocrine or psychiatric diseases and from 2 patients aged 40 and 70 years with secondary hyperparathyroidism due to renal insufficiency. They underwent routine diagnostic lumbar puncture because of suspected prolapse of a disc. Total calcium (Ca) and magnesium (Mg) were also determined in these samples by complexometry . The following findings were obtained (ng/ml, median, range in brackets): Plasma PTH 1.7 (0.7-6.6); CSF PTH 0.8 (0.5-2.3), respectively. No correlation was found between PTH concentrations in plasma and CSF in all 74 samples. The Ca concentrations in plasma, with a median of 2.3 mmol/l (2.1-2.6) were significantly higher than the Ca concentrations in CSF (median 1.1 mmol/l, range 0.4-1.3). The correlation between PTH and calcium levels in CSF was only weak (r = 0.284 P less than 0.05). The Mg levels in CSF (median 1.1 mmol/l, range 0.7-1.6) were higher than Mg concentrations in plasma (median 0.9 mmol/l, range 0.6-1.1). No correlation was found between PTH and Mg in CSF. Our study demonstrated that in man PTH is a normal constituent of CSF.

Dietary carbohydrates effects upon magnesium metabolism in sheep.

Apparent magnesium (Mg) absorption was measured in mature sheep fed hay or vegetative grass, each with and without supplemental glucose (water-soluble carbohydrate). Glucose supplemented in varying levels to hay increased apparent Mg absorption (linear, P less than 0.01) and urinary-Mg output (linear, P less than 0.01). Glucose added to vegetative grass did not change Mg absorption, but plasma-Mg concentrations were higher (P less than 0.05) than controls. Absorption and urinary loss of Mg were positively correlated (P less than 0.01) when hay or grass was fed, with or without glucose. Varying dietary glucose levels in hay or grass did not influence (P greater than 0.05) apparent absorption of calcium (Ca), potassium (K), or phosphorus (P). This study suggests that supplementation with a readily available carbohydrate during periods of dietary Mg deficiency may reduce the rate of plasma-Mg decline characteristic of ruminants grazing spring grass.