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Neutralization of acid in the rumen by magnesium oxide and magnesium carbonate.

Two reagent and two feed grade magnesium oxides and reagent grade magnesium carbonate, sodium bicarbonate, and calcium carbonate were evaluated to ascertain their ability to neutralize acid in the rumen. Rumen fluid pH was increased in vitro, compared to the control, by antacid compounds, and their increased ranked: calcium carbonate less than feed grade magnesium oxide A less than light magnesium oxide and feed grade magnesium oxide B less than heavy magnesium oxide less than magnesium carbonate less than sodium bicarbonate. Titrations at constant pH's ranging from 3.0 to 7.5 indicated that these magnesium compounds were reactive at pH's normally in the rumen although reactivity decreased with increasing pH. Intraruminal doses of feed grade magnesium oxide A and calcium carbonate did not change rumen fluid pH for other compounds ranked: feed grade magnesium oxide B less than magnesium carbonate less than heavy magnesium oxide. Feeding of heavy magnesium oxide or magnesium carbonate increased rumen fluid pH as compared to the control diet. Feeding feed grade magnesium oxide B in three quantities to cattle resulted in proportional increased in fecal pH and fluidity of feces. Two feed grade magnesium oxides differed in their ability to neutralize acid in the rumen.

Animals↗

Bioavailability of magnesium in beef cattle fed magnesium oxide or magnesium hydroxide.

Two experiments were conducted to compare Mg bioavailability from Mg oxide (MgO) vs Mg hydroxide (Mg(OH)2) fed in either a completely mixed diet or a mineral supplement. In Exp. 1, these Mg sources were incorporated into completely mixed diets and offered to 15 steers (282 kg) allotted to three treatments: control diet containing .19% Mg, control plus .2% added Mg as MgO, or control plus .2% added Mg as Mg(OH)2. Each calf was fed 5 kg/d of the respective diet during 10-d adjustment and 7-d collection periods. Blood samples were collected on d 1, 3 and 7. Mg supplementation increased (P less than .01) fecal and urinary Mg excretions, whereas apparent Mg absorption (%) and retention were similar (P greater than .10) for all treatments. Plasma Mg concentrations were similar (P less than .10) for calves supplemented with MgO and Mg(OH)2 but were higher (P less than .05) for Mg supplemented than for control calves on d 7. In Exp. 2, these Mg sources were incorporated into mineral supplements and offered free choice to 30 spring-calving beef cows gazing tetany-inducing pastures from March 6 to May 1. Each of three groups of 10 cows was assigned to a 5.7-ha tall fescue pasture and offered either a control supplement or a supplement containing 40% MgO or Mg(OH)2. Blood samplers were collected on d 0, 7, 14, 28, 42 and 56. Plasma Mg concentrations were not different (P greater than .10) for cows offered MgO and Mg(OH)2 but were higher (P less than .01) for Mg-supplemented than for control cows on d 28, 42 and 56.(ABSTRACT TRUNCATED AT 250 WORDS)

Absorption↗

Intraluminal and contraluminal magnesium on magnesium and calcium transfer in the rat nephron.

Magnesium and calcium transport was studied in the superficial proximal tubule, loop of Henle, and superficial distal tubule of the rat by in vivo microperfusion. Magnesium chloride was used to vary plasma and perfusate magnesium concentration. Perfusion with magnesium-free Ringer solution resulted in little magnesium entry into the tubule lumen in either normomagnesemic or hypermagnesemic rats. Magnesium concentration increased with water abstraction along the perfused proximal tubule whether markedly above or below plasma concentrations. Absolute proximal magnesium reabsorption increased with perfusate concentration; however, fractional magnesium and calcium reabsorption decreased in proportion to net sodium reabsorption with elevated extracellular magnesium. Magnesium absorption increased in the loop of Henle proportional to luminal magnesium concentration. Sodium and calcium reabsorption was not affected. Acute elevation of plasma magnesium, however, significantly depressed absolute magnesium reabsorption to a greater degree than calcium whereas sodium was unchanged. The effects of extracellular magnesium onloop reabsorption were reflected in the final urine. Reabsorption of sodium, calcium, and magnesium in the perfused distal tubule was concentration-dependent and not altered by luminal or extracellular magnesium concentration.

Animals↗

Blood and urinary magnesium kinetics after oral magnesium supplements.

A study was conducted to compare the pharmacokinetic profile of three oral magnesium supplements--magnesium chloride solution, slow-release magnesium chloride tablets, and magnesium gluconate tablets--at 16 mmol/dose. Twelve healthy normomagnesemic subjects were evaluated during an initial baseline study, followed by three magnesium supplementation studies. Supplements were administered in a randomized, crossover fashion at weekly intervals. During each of the four trials, subjects followed the same routines and consumed identical diets. Magnesium concentrations were measured in urine samples collected from 0 to 4, 4 to 8, 8 to 12, and 12 to 24 hours. Intraleukocyte, total serum, and ultrafiltrable magnesium were measured in blood samples drawn at 0, 1, 2, 3, 4, 8, 12, and 24 hours. Compared with baseline, 24-hour urinary magnesium excretion significantly increased (P < 0.05) after the administration of the magnesium chloride solution and also increased after the administration of the other supplements, but the difference was not significant. The 24-hour areas under the curve (AUCs) for total serum, ultrafiltrable, and leukocyte magnesium were greater after the administration of each of the supplements when compared with baseline, although the differences were not statistically significant. Differences in delta AUCs (supplement AUC minus baseline AUC) for total magnesium, ultrafiltrable magnesium, and 24-hour urinary magnesium excretion were statistically different from zero or between supplements. Statistically significant differences (P < 0.05) in total serum, ultrafiltrable, and leukocyte magnesium concentrations were observed at various time points. These results suggest that there were no major differences in the overall effect of these supplements on total serum, ultrafiltrable, and leukocyte magnesium concentrations but do reveal differences in the time-concentration profiles in magnesium levels in blood and urine among the three supplement forms.

Administration, Oral↗

Response of milking cows fed a high concentrate, low roughage diet plus sodium bicarbonate, magnesium oxide, or magnesium hydroxide.

To determine the ability of mineral supplements to elevate depressed milk fat percent, we placed 42 Holstein cows in early to midlactation in seven blocks and assigned each to one of six treatments: control (25% corn silage and alfalfa haylage, 75% concentrate, mostly corn, dry matter); control plus magnesium oxide ground to pass a .425-mm sieve; control plus prilled magnesium oxide sieved to between 1.70 and .425 mm; control plus sodium bicarbonate; control plus reactive powdered magnesium oxide to pass a 45 microns sieve; and control plus powdered magnesium hydroxide. Sodium bicarbonate was 1% of diet as fed, magnesium oxide .5%, magnesium hydroxide .7% later reduced to .5%. Cows were fed control ration for 3 wk to induce milk fat depression, then were changed to treatment rations for 5 wk. Five cows (unblocked) were continued on each dietary treatment for a digestibility study after the feeding trial. All mineral supplements produced greater milk fat percent and yield of milk fat per day than control and all magnesium treatments produced greater milk fat percent than sodium bicarbonate. Magnesium oxide passing a .425-mm sieve produced the greatest increase of milk fat percent. Milk production was most for sodium bicarbonate treatment. Supplementation with magnesium increased ruminal magnesium concentration by factors of 1.26 to 3.75. Blood serum, urine, and fecal magnesium concentrations and fecal pH were more for cows fed magnesium than those fed sodium bicarbonate treatments. Kidney filtration ratios of element to creatinine increased for magnesium when diets were supplemented with magnesium and increased for phosphorus and sodium when diets were supplemented with sodium bicarbonate.

Animal Feed↗

A magnesium load test in the diagnosis of magnesium deficiency.

The concentration of magnesium in muscle was determined and a standardized magnesium load test was performed in 21 patients, who 4 to 10 years previously had undergone intestinal bypass operations for severe obesity. The plasma concentration and 24-h urinary excretion of magnesium were also studied. Basic urinary excretion of magnesium and muscle magnesium were significantly lower in patients compared to healthy controls, while no differences were found in plasma magnesium. A slight negative correlation between muscle magnesium and retained magnesium was demonstrated (r = -0.51, P less than 0.05). Patients with magnesium retention greater than 20 per cent showed a significant decrease of magnesium retention after treatment with magnesium chloride mixture. Four patients with primarily low muscle magnesium all demonstrated an increment in the amount of magnesium in muscle after treatment. The load test described can be applied as a screening test in diagnosing magnesium deficiency.

Adult↗

Effect of parathyroid hormone on renal calcium and magnesium reabsorption in magnesium deficient rats.

Tubular magnesium reabsorption was investigated by recollection micropuncture and in vivo microperfusion techniques in acutely thyroparathyroidectomized rats made magnesium deficient by dietary deprivation. Henle's loop which normally reclaims the major portion of filtered magnesium was examined by elevation of intraluminal magnesium concentration. The transport capacity in these conditions was significantly lower in magnesium deficient rats (41%) compared to normal animals (71%) at comparable magnesium delivery rates. Acute infusion of MgCl2 further depressed loop magnesium reabsorption independent of intraluminal magnesium delivery. Parathyroid hormone did not alter magnesium transport capacity in magnesium deficient rats but resulted in enhanced transport in acutely hypermagnesemic deficient rats. Calcium reabsorption followed a similar qualitative pattern as magnesium with respect to loop function and urinary excretion. These results are consistent with a depressed transport capacity for magnesium in the loop of Henle of magnesium deficient rats which is independent of intraluminal magnesium delivery and circulating parathyroid hormone level.

Absorption↗

Fetal ionized magnesium levels parallel maternal levels during magnesium sulfate therapy for preeclampsia.

OBJECTIVE: Little is known about ion regulation in fetuses. Our aim was to determine the effects of magnesium sulfate therapy on ionized (bioactive) magnesium in the cord blood of pregnancies complicated by preeclampsia. STUDY DESIGN: Seventy-four pregnant women were studied (37 preeclamptic and 37 controls matched for maternal age, gravidity, and gestational age). The preeclamptic women received intravenous magnesium sulfate 6 gm load followed by 2 gm/hour for > or = 4 hours; controls were not preeclamptic and received no magnesium. Maternal venous and fetal cord blood samples were obtained from study and control patients and were analyzed for sodium, potassium, total magnesium, ionized magnesium, total calcium, and ionized calcium. Comparisons between the groups were made and analyzed by the Mann-Whitney U test. RESULTS: There were no significant differences between the treatment and control group cord samples with respect to sodium or potassium. However, total magnesium and ionized magnesium were significantly elevated (p < 0.001) in cord samples of the treated group. At the same time ionized calcium and total calcium were reduced. Interestingly, ionized calcium levels were lower in preeclamptic women before magnesium sulfate therapy was begun, whereas total calcium levels were not different. Importantly, there was no difference between maternal and fetal ionized magnesium levels in either treatment or control groups. CONCLUSIONS: In preeclamptic women undergoing magnesium sulfate therapy, ionized magnesium levels in cord blood parallel maternal levels. Before magnesium therapy ionized calcium levels were lower in preeclamptic women than in matched controls. In the presence of elevated magnesium levels ionized calcium appears to be tightly regulated.

Adolescent↗

Interaction of calcium and phosphate decreases ileal magnesium solubility and apparent magnesium absorption in rats.

We tested the hypothesis that increased intakes of calcium and phosphate lower magnesium solubility in the intestinal lumen, causing a decreased magnesium absorption. In in vitro experiments at a constant magnesium concentration, increasing calcium concentrations reduced magnesium solubility. This effect did not occur in the absence of phosphate. Increasing phosphate concentrations decreased the solubility of magnesium in the presence, but not in the absence, of calcium. These results suggest that the formation of an insoluble calcium-magnesium-phosphate complex determines magnesium solubility. To extend this concept to in vivo conditions, rats were fed purified diets containing a constant concentration of magnesium (16.4 mumol/g) but different concentrations of calcium (25, 100 or 175 mumol/g) and phosphate (58, 103 or 161 mumol/g). Increased intakes of calcium decreased magnesium solubility in the ileal lumen and lowered magnesium absorption. The latter result occurred only if the dietary phosphate concentration was at least 103 mumol/g. Increasing dietary phosphate concentrations reduced both magnesium solubility in the ileum and magnesium absorption, but only if the dietary calcium concentration was at least 100 mumol/g. These results support those obtained in vitro. We conclude that increased intakes of calcium and phosphate decrease magnesium absorption by the formation of an insoluble calcium-magnesium-phosphate complex in the intestinal lumen.

Animals↗

Inhibitory effect of soybean protein vs. casein on apparent absorption of magnesium in rats is due to greater excretion of endogenous magnesium.

Apparent magnesium absorption is depressed in rats fed diets containing soybean protein or enriched with sodium phytate or phosphate in comparison with casein, whereas it is raised in rats fed lactose. However, the possibility that changes in apparent absorption are caused by changes in fecal excretion of endogenous magnesium cannot be excluded. We studied the effects of casein, soybean protein, sodium phytate, lactose and phosphate on apparent and true absorption of magnesium. True magnesium absorption was measured with the use of oral and intraperitoneal administration of tracer doses of 28Mg. Fecal excretion of endogenous magnesium was calculated from apparent and true absorption. True magnesium absorption was not affected by either substitution of soybean protein for casein or by the addition of sodium phytate to a diet containing casein. Endogenous magnesium excretion in feces was significantly increased by soybean protein and sodium phytate. Thus the observed impairment of apparent magnesium absorption in rats fed soybean protein or sodium phytate is due to enhanced fecal excretion of endogenous magnesium. With the other dietary treatments, enhanced fecal excretion of endogenous magnesium was not associated with a discrepancy in the effects on apparent and true magnesium absorption. Dietary lactose vs. dextrose and supplemental phosphate both stimulated fecal excretion of endogenous magnesium, but lactose raised both true and apparent magnesium absorption, and phosphate depressed both true and apparent magnesium absorption.

Absorption↗

Renal elimination of magnesium as a parameter of bioavailability of oral magnesium therapy.

Magnesium is an important cation in human physiology, especially in the regulation of membrane proteins, as a cofactor for various enzyme systems and in neuromuscular transmission. Magnesium deficiency leads to severe impairment in muscle function, particularly in cardiovascular diseases. Classical bioavailability studies with magnesium cannot be carried out for several reasons. As the magnesium concentration in plasma is extraordinarily well regulated, renal elimination proves to be the best method to determine the absorption of orally administered magnesium. Magnesium pools must first be filled, and the saturation phase of renal elimination then equals the degree of absorption. This parameter of bioavailability shows the percentage of eliminated magnesium in comparison to the administered dose. Eighteen healthy male volunteers were included in this study to compare 5 mg magnesium-DL-hydrogen aspartate with magnesium-L-hydrogen aspartate. After a saturation phase, the test substances were administered in random order. Blood samples for determination of magnesium concentrations were taken, but no typical pharmacokinetic concentration curves were obtained. The areas under the concentration-time curves were equal for both formulations (x = 40.22 [mval*h/l]). The bioavailability of both substances was determined from the renal elimination. No significant difference was found between both treatments. Bioavailability of 5 mg magnesium-DL-hydrogen aspartate was 44.5% and for magnesium-L-hydrogen aspartate 41.7%. It is evident that this method of magnesium determination is practical, comfortable for volunteers and gives reliable results in comparing the absorption of magnesium formulations.

Administration, Oral↗

Is lymphocyte magnesium concentration a reflection of intracellular magnesium concentration?

Diuretics are known to cause magnesium depletion, and the aim of the present experiment is to establish the relationship between lymphocyte magnesium concentration and intracellular magnesium concentration during chronic diuretic therapy. Studies were conducted in male Wistar rats that were subjected to daily administration of furosemide (2 mg/kg/day IP) for 19 weeks. Clearance measurements were performed during the baseline week and subsequently during the third, seventh, eleventh, fifteenth, and nineteenth weeks in both furosemide-treated (n = 32) and control rats (n = 32). Lymphocyte magnesium concentration was also measured as a determinant of intracellular magnesium concentration. Magnesium concentrations in kidney, bone, skeletal, and heart muscle tissues were also quantitated at week 11 and at the end of the experiment. After 11 weeks of furosemide administration, furosemide-treated rats developed a lower plasma magnesium concentration (0.95 +/- 0.01 mmol/L) compared with that in the control group (0.99 +/- 0.01 mmol/L). This difference persisted from week 11 to week 19 of the experiment. Fractional excretion of magnesium was modestly elevated in the furosemide-treated group. After 7 weeks of furosemide treatment, lymphocyte magnesium concentration decreased significantly in furosemide-treated rats when compared with that in the control group (1.56 +/- 0.09 micrograms/mg protein vs 1.33 +/- 0.07 micrograms/mg protein). During week 19, the lymphocyte magnesium concentration had fallen to 0.75 +/- 0.04 micrograms/mg protein as compared with 1.45 +/- 0.08 micrograms/mg protein in the control rats. There is a significant correlation between lymphocyte magnesium concentration and plasma magnesium concentration. Our present results indicate that during long-term diuretic therapy, lymphocyte magnesium concentration mirrors the reduction in plasma magnesium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

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

The purpose of this study was to compare the efficacy of three dosages of potassium-magnesium citrate in overcoming thiazide-induced hypokalemia and magnesium loss and increasing urinary pH and citrate. Sixty-one normal subjects first took hydrochlorothiazide at 50 mg/d. After 3 weeks of thiazide treatment or earlier if hypokalemia developed, the subjects were randomized to take one of three dosages of potassium-magnesium citrate (K ( 4 ) MgCit ( 2 ) ) for 3 weeks while continuing on the thiazide: 4 tablets per day (24 mEq potassium, 12 mEq magnesium, and 36 mEq citrate per day), 7 tablets per day (49 mEq potassium, 24.5 mEq magnesium, and 73.5 mEq citrate per day), or 10 tablets per day (70 mEq potassium, 35 mEq magnesium, and 105 mEq citrate per day). Outcome measures were changes in serum potassium and magnesium and urinary potassium, magnesium, pH, and citrate. All three dosages of potassium-magnesium citrate significantly increased serum potassium concentration, with >80% of subjects regaining normal values despite continued thiazide therapy. The two higher dosages, but not the lowest dosage, caused a small but significant increase in serum magnesium concentration, while substantially increasing urinary magnesium. All three dosages significantly increased urinary pH and citrate in a dose-dependent manner. The lowest dosage produced increases sufficient to prevent stone recurrence. Side effects of thiazide therapy were ameliorated by the highest dosage but not by the two lower dosages. Potassium-magnesium citrate at a dosage of 4 tablets per day is adequate to correct thiazide-induced hypokalemia and to increase urinary pH and citrate sufficiently for stone prevention. Higher dosages are probably required for the prevention of magnesium loss and adverse symptoms of thiazide therapy.

Adult↗

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↗

Effects of a magnesium-free dialysate on magnesium metabolism during continuous ambulatory peritoneal dialysis.

While the use of magnesium-containing compounds is usually contraindicated in dialysis patients, the risk of toxicity from hypermagnesemia can be reduced by lowering the magnesium concentration in dialysate. We examined the effects of a magnesium-free dialysate on both serum magnesium level and the peritoneal removal rate of magnesium over 12 weeks in 25 stable patients undergoing continuous ambulatory peritoneal dialysis (CAPD). After 2 weeks, the serum magnesium level decreased from 2.2 to 1.9 mg/dL (0.9 to 0.8 mmol/L) (P less than .02) and the peritoneal removal rate increased from 66 to 83 mg/d (2.8 to 3.5 mmol/d) (P less than .05), with both values remaining stable thereafter. There was a strong association between these parameters (r = -0.62, P less than .05), suggesting that the serum magnesium level decreased as a result of the initial increased peritoneal removal rate. For an additional 4-week period, a subgroup of nine patients received magnesium-containing, phosphate binding agents instead of those containing only aluminum. During this phase, serum inorganic phosphorus was well controlled. The serum magnesium level increased only from 1.8 to 2.5 mg/dL (0.7 to 1.0 mmol/L) (P less than .05), due in great part to the concomitant 41% rise in peritoneal magnesium removal from 91 to 128 mg/d (3.8 to 5.3 mmol/d) (P less than .05). No toxicity was noted during the entire 16-week study period, nor did serum calcium change. Thus, serum magnesium levels remained within an acceptable range as magnesium-containing phosphate binders were given through the use of magnesium-free peritoneal dialysate.(ABSTRACT TRUNCATED AT 250 WORDS)

Aluminum Hydroxide↗

Intravenous magnesium sulfate does not increase ventricular CSF ionized magnesium concentration of patients with intracranial hypertension.

Magnesium sulfate has attracted interest as a potential neuroprotectant but passage of magnesium ion into the central nervous system has not been well documented. For this study, we quantified plasma and cerebrospinal fluid (CSF) ionized magnesium concentration after systemic magnesium sulfate infusion in patients with intracranial hypertension. Patients ( N = 9) received an intravenous infusion of 5 g/20 mmol magnesium sulfate (125 mL of a 4% wt/vol solution) over 30 minutes. Before and after dosing, CSF (from an indwelling ventricular catheter) and blood samples were collected at hourly intervals. Ionized magnesium concentration in all samples was determined using an electrolyte analyzer. Baseline plasma and CSF ionized magnesium concentrations were 0.58 +/- 0.05 and 0.82 +/- 0.06 mmol/L, respectively. Intravenous magnesium sulfate infusion significantly increased plasma ionized magnesium concentration (peak, 0.89 +/- 0.11 mmol/L), but CSF magnesium levels did not change during the 4-hour study. Systemic administration of magnesium sulfate failed to increase CSF ionized magnesium concentration in patients with intracranial hypertension despite increasing plasma magnesium levels by >50%.

Adolescent↗

[Total and ionized magnesium concentration in the blood plasma and erythrocytic magnesium concentration of women in the third trimester of pregnancy with imminent preterm labor].

OBJECTIVES: There are some data concerning magnesium concentration influence on the risk of preterm labor. The estimation of magnesium concentration changes may be useful in prevention of preterm labor. DESIGN: Therefore the aim of our study was to find out the correlation between magnesium concentration and the risk of preterm labor. MATERIALS AND METHODS: Total magnesium concentration and ionized magnesium concentration in blood plasma and erythrocytic magnesium concentration ware examined in the three groups of: 23 women in the third trimester of pregnancy with imminent preterm labor under tocolytic therapy; 20 women in the third trimester of physiologic pregnancy and 19 non-pregnant healthy women in the reproductive age. RESULTS: We discovered statistically confirmed differences (p < 0,05 ) in ionized magnesium concentration as well between the group of women in physiologic pregnancy and non-pregnant women and between the group of pregnant women with imminent preterm labor and non-pregnant women. CONCLUSIONS: Although there were no statistically confirmed differences in total magnesium concentration and erythrocytic magnesium concentration between the three groups of examined women, there were statistically confirmed differences in ionized magnesium concentration between the pregnant and non-pregnant women. Our results suggest that ionized magnesium concentration is better indicator of magnesium balance in human's body than total magnesium concentration.

Adolescent↗

Magnesium status and the effect of magnesium supplementation in feline hypertrophic cardiomyopathy.

Magnesium deficiency has been associated with the development of cardiovascular disease in several species. Cats may be predisposed to alterations in magnesium status because of recent changes in the composition of commercial feline diets. The purposes of this study were 1) to examine the dietary history of cats with hypertrophic cardiomyopathy (HCM), 2) to study magnesium status of cats with HCM compared to normal cats, and 3) to determine the effects of magnesium supplementation in cats with HCM. In part 1 of the study, diets of 65 cats with HCM were examined retrospectively. Forty of the 45 cats for which diets could be determined (89%) ate a diet designed to be magnesium-restricted and/or to produce an acidic urine. In part 2 of the study, 10 cats with HCM were compared to 10 healthy control cats for serum creatinine and magnesium; urine creatinine and magnesium, urine specific gravity and pH, and fractional excretion of magnesium. Urine creatinine and specific gravity were higher in control cats than in cats with HCM. No other differences were found between the 2 groups. In part 3, cats with HCM were supplemented with either 210 mg magnesium chloride (n = 15) or 210 mg lactose (n = 15) for 12 wk. No differences between the 2 groups were found for changes in either magnesium status or echocardiographic parameters. However, the 30 cats with HCM, as a group, did show significant improvements in measures of cardiac hypertrophy over the 12-week period. This was likely the result of treatment with other medications, rather than the magnesium supplementation. The results of this study suggest that cats with HCM are likely to be fed magnesium-restricted diets, but that they do not appear to have altered magnesium status compared to healthy controls.

Animals↗