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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↗
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↗
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

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↗
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

Effect of magnesium deficiency and parathyroid hormone on cyclic AMP metabolism in rat renal cortex.

The influence of magnesium deficiency on cyclic AMP metabolism was investigated in rats on diets of normal and low calcium content. Magnesium deficiency itself did not significantly affect either the basal concentration or the parathyroid hormone-stimulated formation of cyclic AMP in the renal cortex. Magnesium-deficient rats with hypercalcaemia excreted more cyclic AMP in the urine, but similar rats that developed hypocalcaemia on low calcium intake excreted less than their respective controls. The former type of animals also tended to accumulate more cyclic AMP in the renal cortex in response to the injection of a standard dose of parathyroid hormone, whereas rats of the latter type accumulated less. The activity of parathyroid hormone-stimulated renal cortical adenylate cyclase in vitro was increased by magnesium and reduced by calcium under most conditions, but with low concentrations of magnesium small amounts of calcium had a stimulatory effect. These observations suggest that cyclic AMP metabolism is influenced by metabolic disorders developing secondary to magnesium deficiency.

Adenylyl Cyclases↗
PubMed1979

Cell population kinetics and biochemical changes in the rat stomach during magnesium deficiency.

Cell populations of rat stomach have been counted following varying (4-60 days) periods of magnesium-deficient diet and compared to a control group. The activity of beta-glucuronidase and the serotonin concentration were assayed in magnesium-deficient and control rats within four weeks. In the rat stomach the magnesium deficiency produces a numerical decrease in mucous cells, especially marked after 3 and 4 weeks. At this time, the activity of beta-glucuronidase decreases significantly. The concentration of serotonin increases at an earlier time and this increase coincides with the onset of the typical erythema occurring in magnesium-deficient rats.

Animals↗
PubMed1975

Postoperative magnesium deficiency.

Prolonged nasogastric suction and the administration of magnesium-free parenteral fluids produced magnesium deficiency in a patient in the postoperative period. The symptoms of magnesium deficiency are usually overshadowed by those of the primary disease and diagnosis usually rests on the demonstration of low blood concentrations of the ion. Magnesium replacement must be kept in mind when treating patients with intravenous fluids for prolonged periods.

Colectomy↗
PubMed1979

Effects of magnesium deficiency on parturition and uterine involution in the rat.

The effects of moderate magnesium deficiency on the outcome of pregnancy, the process of parturition and uterine involution, were studied in successive experiments using Sherman rats. Females were fed purified diets containing 0.110 or 1.500 g Mg/kg throughout pregnancy and lactation. This magnesium deficient diet decreased the plasma magnesium but did not affect the number of pregnant rats or the weight of females at parturition. There was no change in the weight and size of litter. The number of still births was not significantly increased. The parturition process was observed; abdominal contractions were less obvious in deficient animals than in controls, and they were often not noticeable. Parturition was slightly lengthened in deficient rats. The major effects of magnesium deficiency occurred during lactation when the dam lost weight and the growth of her young was reduced. The uterine weight and its collagen content was higher and the collagen solubility was lower in the deficient rats than in controls between 2 and 10 days post partum. The delay in uterine involution could be prevented by provision of a magnesium supplement after parturition.

Animals↗
PubMed1979

Metabolic performance and GI function in magnesium-deficient rats.

A quantitative evaluation of the mass balance and GI motor effects of dietary magnesium deficiency in the adult male Sprague-Dawley rat is described. Seventy-seven animals were used. Both sham control and experimental groups were maintained on a commercial stock laboratory diet ad libitum for 30 days, after which the experimental rats were switched for 30 days to magnesium-deficient diet ad libitum, containing a magnesium concentration of 16.2 ppm. Ten rats were used to determine the acetylcholine responsiveness of duodenal muscle segments in vitro. In all cases, the segments from the deficient rats were hyperresponsive to a fixed acetylcholine dose. Forty-six rats were used to determine the average intestinal transit rate, which increased significantly in 30-day magnesium-deficient rats. A final series employed 21 rats who were housed in individual metabolic cages. After 5 days on the deficient diet, the average daily fecal pellet counts and fecal weights were significantly reduced. It is concluded that chronic magnesium deficiency is associated with altered GI motor function in the adult male rat.

Animals↗
PubMed1978

Parathyroid hormone secretion in magnesium deficiency.

The effect of an acute elevation of the serum magnesium concentration on the concentrations of serum immunoreactive parathyroid hormone (IPTH) were studied in hypocalcemic hypomagnesemic patients, hyperparathyroid patients, and normal individuals. Basal serum IPTH concentrations in the hypomagnesemic patients ranged from undetectable to 3 times the upper limit of normal. All hypomagnesemic patients were observed to have an immediate rise in the serum IPTH concentration after magnesium administration regardless of the basal IPTH concentration. In contrast, normal individuals and patients with primary and secondary hyperparathyroidism responded to magnesium administration with either a decrease or little change in the serum IPTH concentration. These date indicate that an acute stimulation of PTH secretion induced by magnesium is characteristic of the magnesium-deficient state. The consistency of this response suggests that impaired PTH secretion is a significant factor contributing to the hypocalcemia of magnesium deficiency.

Calcium↗
PubMed1977

Cytoenzymatic studies on the lymphocytes of peripheral blood and lymphatic nodes of rats in an experimental magnesium deficiency.

Wistar rats kept on a magnesium deficient diet show several changes in the lymphatic organs as well as some disorders in the function of the immunological system, which appear as an impairment of cellular immunity and also as hypogammaglobulinemia. In the present experiment the level of leuco- and lymphocytosis has been studied. Furthermore, the activity of some lysosomal enzymes in blood lymphocytes, as well as the ability to incorporate labelled leucine shown by lymph nodes lymphocytes of deficient rats have been investigated. The rise in leuco- and lymphocytosis is similar to that reported by other authors. A significant rise in the activity of beta-glucuronidase as well as a considerable drop in the percentage of enzyme-negative lymphocytes have been observed as early as the first week of experiment. Tissue cultures of the lymph nodes, lymphocytes of deficient rats showed significantly lower values of labelled leucine incorporation with respect to the controls; in contrast, after phytohemagglutinin M stimulation the increase of incorporation in the lymphocytes of deficient and control rats was similar. Our findings may be indicative of some disorders in the redistribution of T and B lymphocytes in the blood and tissues of deficient rats. The observed cytochemical changes may be due to the intensification of autophagic processes in the lymphocytes that manifest a diminished ability to synthetize proteins.

Animals↗
PubMed1975

Depressed immune response in the magnesium-deficient rat.

The effects of dietary magnesium on growth, food efficiency, organ development, splenic nucleic acids, and serum antibody were studied in two experiments with male Wistar rats. Diets containing 30% protein from casein were fed ad libitum. Rats were immunized intravenously with sheep red blood cells. Blood was obtained 5 and 9 days after immunization. In experiment 1, a group of weanling rats was fed 10 ppm Mg for 8 days, followed by 142 ppm for 37 days. Group 2 (controls) was fed 480 ppm Mg for 45 days. Group 1 weighed less but had larger spleens, kidneys, and testes relative to body size than did group 2. Nucleic acids per gram spleen were similar in both groups as were serum gamma-globulin and its 19S and 7S components. Antibody log titers for group 1 were 45 and 65% of control agglutinin levels and 44 and 80% of control hemolysin values on days 5 and 9, respectively. In experiment 2,200-g rats were fed 10 (group 3) or 480 ppm (group 4) Mg for 38 days. Most effects of the 10 ppm Mg diet were similar to those seen in magnesium deficiency in experiment 1. Antibody titers for group 3 were 30 and 25% of control agglutinin and 43 and 53% of control hemolysin values on days 5 and 9, respectively. Total serum gamma-globulin and its 19S fraction were similar in both groups, while the 7S fraction of group 3 was only 64% of the control value.

Animals↗
PubMed1976

Impaired release of parathyroid hormone in magnesium deficiency.

Parathyroid hormone release and end-organ responsiveness to parathyroid extract (PTE) were evaluated in a 25-year-old woman with magnesium deficiency associated with hypocalcemia and inappropriately low levels of serum immunoreactive parathyroid hormone (iPTH). End-organ responsiveness to PTE was demonstrated by increases in serum calcium and in urinary phosphorus, cyclic AMP, and hydroxyproline. When the serum calcium was increased from a baseline of 6.9 mg/100 ml to levels of 8.0 mg/100 ml and higher by calcium infusion, the serum iPTH decreased from the low normal range to below the limits of detectability. The intravenous administration of 3 mg/kg of body weight of magnesium led to an abrupt and striking increase in circulating iPTH with a 2-fold increase in one minute, a 6-fold increase in two minutes, and an 8-fold increase in five minutes. The very rapid increase in serum iPTH produced by magnesium infusion in this study suggests an effect of magnesium on hormone secretion rather than an effect on hormone synthesis. The evidence provided by this investigation indicates that the release of parathyroid hormone is impaired in magnesium deficiency and that the level of circulating calcium required for the suppression of parathyroid hormone secretion is lower than that in normal subjects.

Adult↗