Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Magnesium Deficiency”

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.

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

At least 19 recordsLinked to original sources
PubMed1978

Survival of normal and magnesium-deficient erythrocytes in rats: effect of magnesium-deficient diet vs. splenectomy.

Magnesium deficiency in rats causes anemia, the mechanism of which is unknown. The effect of dietary magnesium, splenectomy, and magnesium content of erythrocytes on erythrocyte survival was studied in Fisher rats. Half of the animals were splenectomized, the remainder sham-splenectomized; each group was subdivided, and some were placed on a magnesium-deficient diet, the rest on a control diet. After 6 weeks, each of the four subgroups was divided, half were given 51Cr-labeled red cells from magnesium-deficient rats, the remainder, labeled normal red cells. The survival functions of the labeled erythrocytes were fitted to a mathematical model composed of both first-order and accelerating components. The results show that the most important factor influencing erythrocyte survival was dietary magnesium intake. The magnesium content of the transfused red cells affected erythrocyte survival only in the rats fed the control diet, whereas splenectomy affected erythrocyte survival only in rats receiving the magnesium-deficient diet. The accelerating component of the survival function was increased eightfold in the animals fed the magnesium-deficient diet, whereas much smaller changes occurred in the first-order components.

Animals↗
PubMed1992

[Heart rate disorders in potassium and magnesium deficiency].

Potassium and magnesium deficiencies are common in patients with heart disease. These are often coexistent and pathophysiologically related. Potassium deficiency cannot be treated without correction of concomitant magnesium deficiency. Correlations between serum levels and body stores are very poor for both ions. Therefore diagnosis and treatment of these conditions based on serum levels alone are erroneous. There is some evidence that it is primarily the intracellular depletion of these ions which is arrhythmogenic. Magnesium infusion has been proved effective in treatment of torsade de pointes ventricular tachycardia and arrhythmias induced by digoxin-intoxication, and is recommended in these conditions. Whether it is effective in other forms of arrhythmia is not yet elucidated.

Action Potentials↗
PubMed1975

The skin in magnesium-deficient rats.

The cutaneous vasodilatation occuring in the early stages of dietary deficiency of magnesium has been investigated in rats. While the time of onset of erythema varies in proportion to the weight of the animal, the duration is not related to weight. In severe states of vasodilatation, the skin is thickened and infiltrated with mononuclear cells, apparently derived from the blood. Intact sympathetic and sensory innervation are not necessary for the development of vasodilatation in the skin. Neither can the genesis of the erythema be attributed to degranulation of mast cells. From consideration of this and other investigations, it is concluded that the cutaneous abnormalities of magnesium-deficient rats cannot be due directly to hypomagnesaemia.

Animals↗
PubMed1975

Ultrastructural changes of the hypothalamo-hypophysial neurosecretory system in the magnesium deficient rats.

A magnesium deficient diet caused transient but marked degenerative changes in the rat hypothalamo-hypophysial neurosecretory system which strongly resembled in many ultrastructural respects those induced by a prolonged administration of aldosterone as previously reported by us. The possible mechanism for this selective alteration in the neurosecretory neurons has been briefly discussed with regard to aldosterone secretion.

Acid Phosphatase↗
PubMed1976

Teratogenic effects of magnesium deficiency in rats.

The effect of severe magnesium deficiency on plasma magnesium levels in pregnant and nonpregnant rats and on reproduction was investigated. Magnesium deficiency produced a rapid fall in plasma magnesium concentration, in both pregnant and nonpregnant rats. At term, all implantation sites of pregnant rats fed a diet severely deficient in magnesium showed total fetal resorption. When pregnant females were fed the magnesium deficient diet only between days 6 and 14 of gestation, there was a high incidence of resorptions and gross malformations were seen in full term fetuses. The results demonstrate the rapidity of the effects of severe magnesium deficiency in pregnant rats and indicate the importance of the element for embryonic development.

Animals↗
PubMed1975

Bone composition and phosphatase activity in magnesium deficiency in rats.

The effect of magnesium deficiency on phosphatase activity and bone composition was determined in the femora of young rats. In the right distal metaphysis the acid and alkaline phosphatase activities were decreased in magnesium-deficient rats, and the activity of bone alkaline phosphatase in the incubation mixture after adding magnesium was significantly greater in the magnesium-deficient than in the control rats. In the left distal metaphysis the water content was significantly lower in the magnesium-deficient rats at the fifth week but not at the third week. Conversely, the ash content of metaphyseal bone was significantly increased in magnesium-deficient rats at the fifth week, but not at the third week. The magnesium and phosphorus contents were abnormally low in the deficient bone at both periods. The calcium content was increased in the deficient bone at the third week, but not at the fifth week.

Alkaline Phosphatase↗
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↗
PubMed1977

Magnesium deficiency anemia in the rat fetus.

Magnesium-deficient fetuses exhibited malformations (44%), anemia, and edema. Maternal plasma magnesium levels at day 21 of pregnancy reflected the level of dietary magnesium (2.43 +/- 0.09 mg Mg/100 ml, control; 0.74 +/- 0.02 mg Mg/100 ml, deficient). Plasma magnesium levels of deficient fetuses showed similar decreases although all fetal magnesium values at term were hihger than maternal values from the same group (3.29 +/- 0.22 mg Mg/100 ml, control; 1.78 +/- 0.07 mg Mg/100 ml, deficient). Magnesium deficiency did not appear to affect the maternal blood parameters. However, when fetal blood was examined, all of the parameters measured were altered in magnesum-deficient fetuses (Table 2). No abnormalities in hemoglobin bands or plasma proteins were seen between any groups by electrophoresis. Measurement of total protein contents showed no differences between maternal blood protein contents, but total plasma protein from magnesium-deficient fetuses was significantly lower than controls (2.00 +/- 0.14 versus 2.62 +/- 0.13 g/100 ml), thus establishing a factor in fetal edema production. Morphologic data showed that in magnesium-deficient fetuses, fetal erythropoiesis was significantly greater in liver, adrenal glands, and spleen than in controls and that maturation was normoblastic. Stained and unstained peripheral blood smears of magnesium-deficient fetuses showed and obvious macrocytosis and at least 50% of the red cells stained abnormally, exhibiting pale areas. Erythrocytic morphology seen in fetal magnesium deficiency is consistent with inadequate filling of the cell by hemoglobin as suggested by Cohlan et al. (5), a probable cause of membrane collapse. The inadequate filling of magnesium-deficient red blood cells (RBC) with hemoglobin might be explained by a reduction in hemoglobin synthesis which is consistent with the reduced mean corpuscular hemoglobin (MCH) and MCH concentration (MCHC) of the deficient fetal red cells. The role of magnesium in protein synthesis is also compatible with a reduction in hemoglobin synthesis, yet may not completely explain the abnormalities and resultant shortened lifespan of the red cells.

Anemia↗
PubMed1977

Erythrocyte membrane plaques from rats with magnesium deficiency.

This study investigated the anemia of dietary magnesium deficiency in inbred Fisher white rats using freeze-fracture electron microscopy. The plasma membranes of erythrocytes from animals receiving two different magnesium-deficient and control diets were observed at weekly or biweekly intervals for 6 wk. The earliest changes were small plaques on the external surface (ES) and fracture face (PF) of erythrocyte plasma membranes, which occurred after 2 wk of either magnesium-deficient diet. These plaques persisted and increased in size with progressive magnesium deficiency. When fully developed, the plaques consisted of round or oval elevations approximately 30-50 nm in diameter outlined by a narrow raised border. The surface of the plaques was smooth and devoid of intramembranous particles. Incubation of erythrocytes from magnesium-deficient rats in a physiologic solution containing 2 meq/liter magnesium for 1 hr at 37degrees C did not alter the appearance of the plaques. Erythrocytes from control rats, obtained during the same time periods, showed no plaques. Thus, a deficiency of magnesium in rats altered erythrocyte membrane structure.

Animals↗
PubMed1976

Functional hypoparathyroidism and parathyroid hormone end-organ resistance in human magnesium deficiency.

Hypocalcaemia is a well-recognized manifestation of magnesium deficiency. We have studied seventeen patients with this syndrome in an attempt to determine the pathogenesis of the hypocalcaemia. Mean initial serum calcium concentration was 5-6 mg/dl and mean initial serum magnesium concentration was 0-75 mg/dl. Serum immunoreactive parathyroid hormone (IPTH) was measured in sixteen patients in the untreated state. Despite severe hypocalcaemia, serum IPTH was either undetectable (less than 150 pg/ml) or normal (less than 550 pg/ml) in all but two patients. Serial measurements made during the initial 4 days of magnesium therapy in four patients showed an increase in serum IPTH within 24h, but a delayed increase in serum calcium, which required approximately 4 days to reach normal values. The effect of the rapid normalization of serum magnesium on serum IPTH and serum calcium concentration was studied in three patients. Within 1 min after 144-300 mg of elemental magnesium was administered i.v., serum IPTH had risen from undetectable to 3600 pg/ml and 1725 pg/ml in two patients and from 425 pg/ml to 937 pg/ml in the third. Serum calcium concentrations were unchanged after 30-60 min. These data provide evidence for impaired parathyroid gland function in most of the magnesium deficient patients. The rapidity with which serum IPTH rose in response to magnesium therapy indicates that this may reflect a defect in parathyroid hormone (PTH) secretion rather than its biosynthesis. The failure of serum calcium concentration to increase during the initial days of magnesium repletion, at a time when serum IPTH concentrations were normal or elevated, suggests end-organ resistance to PTH in these patients. The renal response to PTH was examined in two magnesium deficient patients by measurement of urinary cyclic AMP excretion following administration of parathyroid extract. In both patients there was a minimal increase in urinary cyclic AMP concentrations. In contrast, when the hepatic response to glucagon was tested on the same patients by measurement of plasma cyclic AMP concentrations following administration of glucagon, normal increases were observed. These results suggest that adenylate cyclase systems of various organs may be affected differentially by a state of magnesium deficiency. It is suggested that magnesium deficiency may result in defective cyclic AMP generation in the parathyroid glands and in the PTH target organs. This could be the principal mechanism operative in both impaired PTH secretion and end-organ resistance to PTH which together contribute to the development of hypocalcaemia.

Adult↗
PubMed1992

Magnesium deficiency diagnosed by an intravenous loading test.

Magnesium deficiency is common but difficult to diagnose and to assess in clinical practice. The use of a magnesium loading test was therefore evaluated to diagnose magnesium deficiency in 661 hospitalized patients with medical conditions assumed to interfere with magnesium uptake and excretion. Thirty millimoles of magnesium sulphate were administered intravenously during 8 h as a loading test and related to the urinary excretion in the following 24 h. A group of 30 patients without any known predisposition for magnesium deficiency and a group of 27 healthy volunteers served as controls. The mean (with 95% confidence interval) magnesium retention was 4 (-2-10)% in the control group of patients and 3 (-2-8)% in healthy subjects. A significantly higher retention was observed in all the groups of the patients: atrial fibrillation 18 (11-25)%, other arrhythmias 18 (11-24)%, hypertension 27 (20-33)%, coronary artery disease 25 (20-30)%, congestive heart failure 31 (26-37)%, cerebrovascular events 38 (24-51)%, gastrointestinal disorders 22 (14-29)%, diabetes mellitus 16 (9-22)%, and alcoholics 33 (29-36)%. The percentage of patients with a retention greater than mean + 2 SD of the two control groups varied between 22% and 54% among the different patient groups. The mean serum magnesium among the patient groups was similar to the control group of patients, except for the alcoholics, hypertensives and young healthy controls, who had significantly reduced levels. Magnesium retention was significantly correlated to age and renal function, and among the alcoholics negatively correlated to serum magnesium.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1975

Magnesium deficiency and cardiac disorders.

Magnesium deficiency can occur in congestive heart failure, after diuresis with furoxemide, ethacrynic acid and mercurials, and with digitalis intoxication, diabetic acidosis, acute and chronic alcoholism, delerium tremens, cirrhosis, malabsorption syndromes, protracted postoperative cases, open heart surgery, the diuretic phase of acute tubular necrosis, and with hypoparathyroidism, primary aldosteronism, juxta-glomerular hyperplasia and pancreatitis. Two cases of serious ventricular arrhythmias associated with magnesium depletion are described. Clinical manifestations are vague but center around neurologic symptoms such as weakness, tremors, stupor, coma, nausea, vomiting and anorexia. Serious cardiac arrhythmias also occur with magnesium depletion. Magnesium appears to be very useful in hypomagnesemic or digitalis-toxic tachyarrhythmias. Magnesium may also be valuable in normomagnesemic tachyarrhythmias. Ten to fifteen milliliters of a 20 percent magnesium sulfate solution, given intravenously over 1 minute, followed by a slow 4 to 6 hour infusion of 500 ml of 2 per cent magnesium sulfate in 5 per cent dextrose in water is recommended. Recurrence of arrhythmias is common and a second infusion of magnesium sulfate may be necessary. Hypermagnesemia occurs frequently in renal insufficiency, and magnesium therapy may then be contraindicated. Serum levels above 5.5 meq/liter should be avoided. Loss of deep tendon reflexes and a decrease in respiratory rate can be used as guides to magnesium therapy. A plea is made for frequent analysis of serum magnesium so that more knowledge can be gained regarding this important biologic element in cardiovascular disorders.

Alcoholism↗
PubMed1975

Protective effect of coexistent thiamine deficiency upon the experimental cardiomyopathy associated with acute magnesium deficiency in the Syrian golden hamster.

Repeated efforts to induce beriberi heart disease by experimental thiamine deficiency (B1d) have failed in many species. To test the hypothesis that magnesium deficiency (Mgd) might be the cofactor necessary for heart failure, 10-week-old Syrian golden hamsters were divided into four groups-control (C), B1d, Mgd, and combined MgB1d-and were fed the diets ad libitum for 3 weeks. On day 21, animals were studied under intraperitoneal pentobarbital anesthesia (50 mg/kg). Electrocardiograms were taken and right and left ventricular pressures were measured by transthoracic needle puncture. Cardiac output was measured by the direct Fick method. The complete study was performed in 9 C, 13 B1d, 9 Mgd, and 14 MgB1d animals. B1d was proven by low red blood cell transketolate high B1 pyrophosphate effect, and was accompanied by tachycardia and hypercalcemia. B1 did not differ from C in any other parameter. Mgd was characterized by hypomagnesemia, hypercalcemia, prolongation of the PR interval, widening of the QRS interval, low O2 consumption, low cardiac output, and increased heart weight to body weight ratio (HW/BW) as compared to control. No differences were observed in right and left ventricular pressures or peak /dt. MgB1d was characterized by hypomagnesium, hypercalcemia, low red blood cell transkeotlase, and high B1 pyrophosphate effect. MgB1d minimized the deleterious effects of Mgd: animals were more active and the mortality was low, the PR interval remained normal, the QRS interval widened significantly less, cardiac output remained normal, and HW/BW increased significantly less. Although, once again, beriberi heart disease was not produced, B1d appeared to exert a protective effect upon the Mg-deficient myocardium.

Acute Disease↗
PubMed1975

Mast cell increase in the duodenum and kidney of magnesium-deficient rats.

Rats were maintained on a magnesium-deficient diet for 1 to 5 weeks to study the mast cell (MC) populations in their duodenum and kidney. A marked increase of intestinal subepithelial mast cells was observed in these animals as compared with normal controls. The cells in both groups showed an identical reaction for mucopolysaccharides but the 5-hydroxytryptamine content tended to be higher in the cells of magnesium-deficient animals. Proliferation of MC was also observed in the renal cortex of the magnesium-deficient rats. This finding is significant because MC are known to be virtually absent from normal kidneys. Magnesium deprivation resulted in numerous MC not only in the intertubular spaces but also within the glomeruli. Possible correlations between these and other pertinent observations are discussed with regard to certain renal diseases. The discussion is extended to the possible mechanism through which magnesium could influence secretory processes in MC.

Alcian Blue↗
PubMed1976

The activity of certain hydrolases of rat erythrocytes in experimental magnesium deficiency.

In rats with induced syndrome of chronic magnesium deficiency, occurrence of haemolytic anaemia in conjuction with a shortening of the erythrocyte survival time and marked reticulocytosis among other symptoms became noticeable. In the present experiment the authors undertook to study the behaviour of the lysosomal enzymes in the erythrocytes of magnesium-deficient rats. In these animals anaemia and reticulocytosis as well as a marked increase in the percentage of the erythrocytes showing positive reactions to the acid phosphatase and beta-glucuronidase tests developed. It seems likely that the positive lysosomal reactions were obtained with younger blood cells which did not stain with brilliant cresyl blue but still retained single lysosomes in their cytoplasm. This assumption was confirmed by ultrastructural studies which demonstrated the presence of siderosomes inside both the reticulocytes and the mature erythrocytes. The changes in the percentages of reticulocytes and enzyme-positive erythrocytes were independent of the histological structure of the experimental rat's thymus. In the reticulocytes as well as in the mature erythrocytes, the noteworthy presence of degenerated mitochondria containing electron-dense material seems to be a morphological sign of impairment of the magnesium-deficient rat's erythrocytes.

Acid Phosphatase↗
PubMed1978

Effects of magnesium deficiency on duodenal and ileal magnesium absorption and secretion.

Intestinal adaptation by the growing rat to a low-magnesium diet was studied by in situ perfusion of duodenum and ileum in vivo. Rats were fed diets containing either 0.066 or 0.022% Mg for 3 weeks. Magnesium-restricted rats became hypomagnesemic and hypercalcemic. Net magnesium secretion was studied by perfusing an initially magnesium-free saline solution; secretion was higher in duodenum than in ileum, and decreased significantly in the duodenum in response to magnesium restriction. Net magnesium adsorption studied by intraluminal perfusion of 2.5 mM magnesium in saline was greater in duodenum than ileum in rats taking a low-magnesium diet, but duodenal and ileal absorption did not differ in animals taking the normal magnesium diet. Absorption did not adapt significantly to magnesium restriction in either segment. Adaptation of small-intestinal magnesium transport to a low magnesium diet is minimal, consisting mainly of reduced duodenal magnesium secretion.

Animals↗
PubMed1975

The effect of magnesium deficiency in mice on serum immunoglobulin concentrations and antibody plaque-forming cells.

Magnesium-deficient mice immunized with SRBC showed a significant decrease (P less than 0.001) in the number of PFC in their spleens compared with mice on a control diet. Serum immunoglobulin concentrations (IgG1, IgG2, IgA and IgM) were determined after 3, 6, 9 and 12 days on the respective diets. The serum IgG2 and IgM concentrations of magnesium- deficient mice were decreased (P less than 0.005) by 6 days and remained at these concentrations until 12 days. The serum IgG1 and IgA concentrations of magnesium deficient animals also decreased (P less than 0.01) by 6 days but returned toward control concentrations at 12 days. Serum magnesium concentrations confirmed the magnesium deficiency of the experimental animals. Therefore, magnesium deficiency has profound immunosuppressive capabilities in mice by significantly reducing the number of antibody synthesizing cells and serum immunoglobulin concentrations.

Animals↗
PubMedDate not supplied

Propranolol reduces cardiomyopathic injury induced by magnesium deficiency.

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.

Animals↗