Calcium Output Research Articles

Effect of tauroursodeoxycholic acid on bile flow and calcium excretion in ischemia-reperfusion injury of rat livers

Background/Aims: Tauroursodeoxycholic acid is known to have a hepatoprotective action in cholestatic disorders. We evaluated whether oral pretreatment with tauroursodeoxycholic acid could protect the liver from ischemia-reperfusion injury, with particular regard to its effect on bile flow and biliary calcium excretion. Methods: A 1-hour in vivo ischemia-reperfusion model of 70% of the lobes of rat liver was used. Animals were divided into six groups (each group; n=8); a non-ischemia sham group (CS), a control group without bile acids (CON0, and 4 bile acid groups; 10 mg/kg and 50 mg/kg (U10, U50), taurocholic acid 10 mg/kg (CA10) and tauroursodeoxycholic acid 10 mg/kg (CD10). Bile acids were given orally for 7 days before operation. Results: Three hours after reperfusion, oral bile acid pretreatment failed to reduce the hepatic ischemia-reperfusion injury biochemically, but histological improvement was observed in the tauroursodeoxycholic acid groups. After reperfusion, tauroursodeoxycholic acid significantly increased bile flow from the ischemic liver, and also significantly increased serum calcium concentration. Although tauroursodeoxycholic acid did not change biliary calcium concentration, it significantly enhanced total biliary calcium output during reperfusion. Conclusion: Thus, tauroursodeoxycholic acid inhibited tissue calcium accumulation and enhanced sinusoidal and biliary calcium output during hepatic ischemia-reperfusion. However, it is still unclear if calcium mobilization is part of the protective mechanisms of tauroursodeoxycholic acid in ischemia-reperfusion injury of the liver.

Calcium requirements of lactating Gambian mothers: effects of a calcium supplement on breast-milk calcium concentration, maternal bone mineral content, and urinary calcium excretion

The calcium requirement for prolonged lactation was investigated in a randomized supplementation study of Gambian mothers consuming a low-calcium diet (7.1 mmol/d, or 283 mg/d). Sixty women were studied from 10 d to 78 wk of lactation, receiving calcium or placebo for the first 12 mo. The supplement increased average calcium intake by 17.9 mmol/d (714 mg/d). Supplementation had no effect on breast-milk calcium concentration or on maternal bone mineral content. Urinary calcium output was higher in supplemented than in unsupplemented mothers by 1.18 mmol/d (47 mg/d), P < or = 0.005. Longitudinal changes in urinary calcium output and bone mineral content made a substantial contribution to calcium requirements for lactation. This study suggests that, in women with low calcium intakes, there is no direct benefit from increasing calcium intake during lactation, and that physiological mechanisms operate to furnish calcium for breast-milk production.

Hormone-induced bile flow and hepatobiliary calcium fluxes are attenuated in the perfused liver of rats made cholestatic with ethynylestradiol in vivo and with phalloidin in vitro

The actions of vasopressin and glucagon, administered alone or together, were assessed on bile flow in perfused livers from rats made cholestatic by the injection of ethynylestradiol and from those allowed to recover from such treatment. Concomitant measurements were made of biliary calcium output as well as changes in the perfusate Ca2+ concentration, glucose output, and oxygen uptake. Experiments were also conducted where cholestasis was induced in vitro in the perfused liver by the infusion of phalloidin. In each case cholestasis was demonstrated to have occurred by a reduction in bile flow by approximately 50%. The data show that the transient increase in bile flow and bile calcium seen in control rat liver soon after the administration of vasopressin, particularly when coadministered with glucagon, is largely absent in cholestasis induced by ethynylestradiol and attenuated in cholestasis induced by phalloidin. At the same time the pattern of perfusate Ca2+ fluxes in ethynylestradiol-induced cholestasis shifts to one reflecting net efflux of the ion from the liver. The responses to glucagon administration alone contrast with those of vasopressin in that in the perfused liver of ethynylestradiol-treated rats, glucagon induces a pronounced and sustained increase in bile flow. In cholestasis induced by both ethynylestradiol and phalloidin, glucagon fails to induce an initial transient decrease in bile flow. The effects of glucagon, including enhancement of vasopressin-stimulated bile flow in control and in ethynylestradiol-treated rats, can be mimicked by dibutyryl cyclic adenosine monophosphate (cAMP). Changes in glucose output and oxygen uptake induced by both hormones are only slightly attenuated. The data show that the modulation of bile flow that occurs rapidly after the administration of vasopressin and glucagon to control perfused rat liver is altered in conditions of cholestasis induced by either ethynylestradiol or phalloidin.

Hormone-induced bile flow and hepatobiliary calcium fluxes are attenuated in the perfused liver of rats made cholestatic with ethynylestradiol in vivo and with phalloidin in vitro

The actions of vasopressin and glucagon, administered alone or together, were assessed on bile flow in perfused livers from rats made cholestatic by the injection of ethynylestradiol and from those allowed to recover from such treatment. Concomitant measurements were made of biliary calcium output as well as changes in the perfusate Ca 2+ concentration, glucose output, and oxygen uptake. Experiments were also conducted where cholestasis was induced in vitro in the perfused liver by the infusion of phalloidin. In each case cholestasis was demonstrated to have occurred by a reduction in bile flow by approximately 50%. The data show that the transient increase in bile flow and bile calcium seen in control rat liver soon after the administration of vasopressin, particularly when coadministered with glucagon, is largely absent in cholestasis induced by ethynylestradiol and attenuated in cholestasis induced by phalloidin. At the same time the pattern of perfusate Ca 2+ fluxes in ethynylestradiol-induced cholestasis shifts to one reflecting net efflux of the ion from the liver. The responses to glucagon administration alone contrast with those of vasopressin in that in the perfused liver of ethynylestradiol-treated rats, glucagon induces a pronounced and sustained increase in bile flow. In cholestasis induced by both ethynylestradiol and phalloidin, glucagon fails to induce an initial transient decrease in bile flow. The effects of glucagon, including enhancement of vasopressin-stimulated bile flow in control and in ethynylestradiol-treated rats, can be mimicked by dibutyryl cyclic adenosine monophosphate (cAMP). Changes in glucose output and oxygen uptake induced by both hormones are only slightly attenuated. The data show that the modulation of bile flow that occurs rapidly after the administration of vasopressin and glucagon to control perfused rat liver is altered in conditions of cholestasis induced by either ethynylestradiol or phalloidin.

Effect of acute bile acid pool depletion on total and ionized calcium concentrations in human bile*

Although calcium salts are important components of gallstones, there are few data on the total and ionized calcium content of human bile. Therefore, in 14 fasting T-tube patients studied 7-11 days after cholecystectomy, we measured bile flow, bile acid [BA], total [CaTOT] and free ionized [Ca++] calcium concentrations, in 20-30 min bile collections during acute BA pool depletion induced by 6-8 h of continuous bile drainage. During washout of the BA pool there were parallel falls in bile flow, BA output and total calcium output (correlation coefficients ranging from 0.59 to 0.99; P < 0.02-0.001). In 12 of the 14 patients, [CaTOT] also fell (from 1.84 +/- 0.29 to 1.32 +/- 0.34 mmol L-1) in parallel with [BA] (from 34.0 +/- 14.0 to 8.2 +/- 8.0 mmol L-1; r = 0.75-0.98; P < 0.005). In contrast, biliary [Ca++] remained virtually unchanged. These data suggest that the BAs are linked to the bound, rather than to the free, ionized, fraction of biliary calcium, which is consistent with in vivo calcium binding by BAs. A model is proposed in which BA-induced biliary calcium secretion results from (i) bile acid-induced water flow via solvent drag; and (ii) calcium binding in the bile canaliculus by bile acids, which induces paracellular diffusion of Ca++, thereby maintaining [Ca++] independent of [BA].

Hypercalcemia decreases bile flow and increases biliary calcium in the prairie dog

Biliary calcium is known to play an important role in the pathogenesis of gallstones. Calcium salts are present in all pigment gallstones and are also present in the core of most, if not all, cholesterol gallstones. The effects of acute hypercalcemia on bile flow and biliary calcium secretion were examined in 22 prairie dogs during intravenous taurocholate infusion (0, 1.0, 2.25, and 4.5 mumol/kg/min). Bile flow was linearly correlated with bile acid output in both control (y = 7.62x + 13.5, r = 0.98) and hypercalcemic (y = 7.00x + 10.4, r = 0.96) animals. At lower bile acid outputs (< 3.0 mumol/kg/min), biliary ionized calcium output per increment bile acid output was significantly increased in hypercalcemic animals (0.016 versus 0.011 mumol Ca++ mumol taurocholate, p < 0.001). Bile ionized calcium concentrations approximated Gibbs-Donnan predicted values only at low bile flow rate. Hypercalcemia decreases bile flow and increases biliary ionized calcium concentration in the prairie dog. These effects favor the precipitation of calcium salts in bile.

Global Existence Results for a Mathematical Model of Cell Morphogenesis in Calcium-Regulated Strain Fields

The present paper is concerned with the mathematical analysis of a mechano-chemical model describing the dynamics of a cell where calcium input and calcium output processes are involved. In this model the cortical cytoplasm is considered as a (visco)elastic continuum in which calcium ions can diffuse and interact with the cytoskeleton. The evolution of such a medium is described by a nonlinear partial differential equations system, where the balance laws for the concentrations of free calcium and bound (to specific macromolecules) calcium are coupled with the equilibrium equation for the displacement. The existence of a (weak) solution to the corresponding initial-boundary value problem is proved by variational methods. In the strongly viscoelastic case also a uniqueness result is stated. The properties of stationary solutions of the system are discussed.

Potassium depletion and salt-sensitive hypertension in Dahl rats: effect on calcium, magnesium, and phosphate excretions.

Weanling male inbred Dahl rats (Jr salt-sensitive (S) and salt-resistant (R) strains) were placed on high (4%, HK) and low (0.2%, LK) potassium diets for 4 weeks. Both diets contained 8% sodium chloride, 2.5% calcium, 0.8% magnesium, and 2.0% phosphorous. Balance studies were carried out during the final week on the diets. Mean arterial blood pressure was determined, and dietary intake and urinary output of water, sodium, chloride, potassium, calcium, magnesium, and phosphate were monitored daily during this period. The data show that blood pressures of S rats were significantly higher than those of R rats on both HK and LK diets; however, reduced dietary potassium was associated with increased blood pressure in both strains. Urinary excretions of calcium and magnesium were higher, and urinary phosphate excretion was lower, in S compared to R rats. Decreased potassium intake was associated with increased excretion of calcium, magnesium and phosphate in both strains. The changes in calcium and magnesium excretion were significantly correlated to blood pressure across strains and diets. We conclude that the effects of a high salt diet on increasing blood pressure can be potentiated by lack of potassium, even in previously salt-resistant rats. Increased blood pressure is associated with increased divalent cation excretion. It is not yet known whether this is a cause-and-effect relationship.

Calcium requirement—a reappraisal of the methods used in its determination and their application to patients with osteoporosis

The accepted practice of calculating the dietary calcium requirement from the relationship between calcium balance and intake was recently criticized on mathematical grounds. To try to determine the appropriate calcium intake in patients with osteoporosis, I examined the relationships between calcium intake, output, and balance in a group of such patients. Calcium-balance studies were performed on 25 patients with untreated osteoporosis: intake (x +/- SEM) was 30.34 +/- 3.02 mmol/d, output was 30.59 +/- 2.69 mmol/d, and calcium balance was -0.25 +/- 0.64 mmol/d. There was a significant correlation between intake and both output and balance (r = 0.98, P < 0.001 and r = 0.61, P < 0.01, respectively). Intake and output became equal at 31.7 (95% CI 27.9, 35.5) mmol/d. This value is the same as that obtained when the conventional method of calculation is used. Furthermore, if random values for calcium output are assigned to the observed values of intake it can be demonstrated that the same values will always be obtained by both methods The only difference is that the calculation based on balance and intake results in a narrower confidence interval.

Effect of artificial saliva and calcium on fluoride output of controlled-release devices.

The purpose of this in vitro study was to assess the effect of graded concentrations of calcium in artificial saliva on the output of fluoride from HEMA/MMA controlled-release devices. After the initial release rates were determined in deionized water, the devices were assigned to five groups. The devices of one group remained in deionized water throughout the 19-day study while those of the other groups were placed in artificial saliva containing 0, 4.5, 8.0, or 12.0 mg% calcium on days 4-13. Ten devices of each group were placed in deionized water again on days 14-17 and then in 0.1 mol/l HCl on days 18-19. The five devices of each group that were not placed in deoinized water on day 14 were inspected for surface crystals and then placed in 1 mol/l KOH for 2 days. The fluoride release rates in artificial saliva were reduced by 71-90% and in proportion to the calcium concentration. The release rates in deionized water (days 14-17) approached the baseline values; they exceeded baseline rates by 13-49% while in HCl. The fluoride release rates did not differ among the groups while in KOH, but calcium output was directly related to the calcium concentration of the artificial saliva. The results indicate that fluoride release from HEMA/MMA devices is markedly reduced in artificial saliva and that the reduction is proportional to the concentration of calcium.

Calcium intakes and bone densities of lactating women and breast-fed infants in The Gambia.

The calcium required for breast-milk production and infant growth can be a substantial proportion of dietary intakes especially in regions of the world were calcium consumption is low. Insufficient calcium supply might lead to maternal bone loss, reduced breast-milk calcium secretion and impaired infant bone growth. However, changes in calcium absorption and excretion may be sufficient to allow these requirements to be met without affecting maternal or infant health. A limited number of studies have investigated changes in maternal bone mineral, absorption, excretion and metabolism during lactation but few have addressed whether any changes are influenced by calcium intakes. Ongoing detailed research by the MRC Dunn Nutrition Unit in a rural area of The Gambia amongst mothers and infants with habitually low calcium intakes will provide valuable information about calcium needs during lactation and growth.

The Nature and Significance of the Relationship between Urinary Sodium and Urinary Calcium in Women

Orally or parenterally administered sodium is known to increase urinary calcium in experimental animals and humans, and there is well-documented correlation between urinary sodium and calcium in 24-h urine collections from normal subjects and renal stone formers. The correlation between urinary sodium and calcium is generally sodium driven, i.e., it is the sodium load that influences urinary calcium rather than vice versa, but the converse may also occur, as after an oral calcium load or in hypercalcemia. When sodium is the determinant, 100 mmol of sodium takes out approximately 1 mmol of calcium in the urine. When calcium load is the determinant, each millimole of calcium appearing in the urine is associated with an extra 10-20 mmol of sodium. Sodium-dependent calcium loss may continue indefinitely, but calcium-dependent natriuresis is self-limiting. There is a significant correlation between calcium and sodium in fasting urine from both pre- and postmenopausal women, but there is more calcium relative to sodium in postmenopausal women than in premenopausal women. In postmenopausal but not premenopausal women, urinary hydroxyproline is also related to obligatory sodium and calcium output, and restriction of salt intake lowers not only urinary sodium but also calcium and hydroxyproline. There is not only an increase in obligatory calcium excretion at the menopause, but also an increase in the fasting urinary sodium, which in turn accounts for some of the increase in calcium output. This rise in fasting urinary sodium represents a delay in sodium excretion that may have a significant effect on calcium homeostasis.

GLOBAL SOLUTION TO A MODEL FOR CELL MORPHOGENESIS BY CALCIUM-REGULATED STRAIN FIELDS

In this paper we prove an existence and uniqueness result for a time-dependent problem related to a mechanochemical model of cellular morphogenesis, based on calcium ion regulation of the viscoelastic properties of the cellular cortex. Calcium input and output processes, as well as diffusive effects, are accounted in the description of the cell dynamics. The resulting system of nonlinear partial differential equations consists of the balance laws for the concentrations of free calcium and bound (to specific macro-molecules) calcium, coupled with the equilibrium equations for the displacements. It is shown that the initial-boundary value problem has only one solution which satisfies suitable boundedness estimates regarding calcium concentrations.

Calcium homeostasis in pregnant women receiving long-term magnesium sulfate therapy for preterm labor

OBJECTIVES: The hypothesis of this study is that calcium homeostasis and bone mineralization are altered in pregnant women receiving long-term therapy with magnesium sulfate as compared with similar women not receiving magnesium sulfate to control preterm labor. STUDY DESIGN: Thirty-nine women between 24 and 32 weeks' gestation, matched for age, race, and duration of bed rest, were enrolled. Indices of calcium homeostasis in serum and urine were measured serially, and bone mineralization of the distal radius was measured at 1 and 11 weeks post partum. RESULTS: Magnesium therapy was administered for a mean duration of 26 ± 14 days and a cumulative dose of 1405 ± 963 gm. Serum concentrations of magnesium, phosphorus, and parathyroid hormone increased and those of calcium decreased from baseline values in the magnesium sulfate group and remained uniform throughout the 3-week investigation. The serum magnesium, phosphorus, parathyroid hormone, and calcium concentrations in the control group were unchanged during the study and differed significantly from those in the magnesium sulfate group (p < 0.001). Urinary output of magnesium, calcium, and copper was significantly greater in the magnesium sulfate group than in the control group throughout the study. Urinary losses of calcium in the magnesium sulfate group, approximately 800 to 900 mglday, were substantial. Although radius bone density 1 week post partum did not differ between groups, the change in bone density from 1 to 11 weeks post partum was significantly lower in the magnesium sulfate group than in controls. CONCLUSIONS: These data suggest that calcium homeostasis is altered during and after long-term magnesium sulfate therapy. The marked, prolonged urinary calcium losses may affect maternal bone mineralization. (AM J OBSTET GVNECOL 1992;167:45-51.)

Renal excretory profiles of loop diuretics: consequences for therapeutic application.

In healthy subjects, 24-h natriuresis, kaliuresis, calciuresis, and magnesiuresis increase in response to the first oral dose of a standard (diuretic) formulation of a loop diuretic, such as furosemide 40 mg. However, low-dose formulations of loop diuretics, such as torasemide 2.5 mg, do not elevate 24-h natriuresis after the first dose is administered to normal individuals who are in steady-state habitual sodium balance; these formulations of loop diuretics are consequently labeled as nondiuretic formulations (of diuretic substances). Nondiuretic formulations of loop diuretics do not increase the 24-h urinary outputs of sodium, potassium, calcium, or magnesium after the first dose or in the course of repeated once-daily administration to healthy subjects. The 24-h natriuretic response to the first dose of standard (diuretic) formulations of loop diuretics wanes during repeated once-daily administration to healthy individuals, whereas the kaliuretic response becomes slightly attenuated, and calciuresis and magnesiuresis bear little change. Once-daily treatment with any formulation of a loop diuretic may result in an increase in plasma urate concentration. Nondiuretic formulations of loop diuretics, which are efficacious as once-daily monopharmacotherapy for high blood pressure, should be tried before standard (diuretic) formulations of diuretics are used in the treatment of uncomplicated essential hypertension. When loop diuretics are employed in the treatment of congestive heart failure, the minimal dose compatible with the attainment of clinical objectives should be used.

Renal excretory responses to single and repeated administration of diuretics in healthy subjects: Clinical connotations

Administration of an initial oral dose of hydrochlorothiazide 25 mg to healthy subjects is followed by increased 24-hour urinary outputs of sodium, chloride, and potassium. On the fourth day of once-daily dosing with hydrochlorothiazide 25 mg, 24-hour natriuresis and chloriuresis are no longer augmented, but the elevation in 24-hour kaliuresis that follows the first dose remains unchanged. Twenty-four-hour urinary calcium output is consistently reduced during repeated once-daily administration of hydrochlorothiazide 25 mg. The first oral dose of the loop diuretic torasemide augments the average natriuresis and kaliuresis in the 6 hours immediately after dosing in healthy subjects, in a dose-dependent fashion, within the 2.5 to 10-mg range. These increased urinary outputs are followed by rebounds below postplacebo values between 6 and 24 hours after dosing. As a result of this biphasic response, torasemide 2.5 mg qualifies as a nondiuretic formulation (it does not elevate 24-hour natriuresis), whereas torasemide 5 and 10 mg qualify as diuretic formulations. After the seventh dose of torasemide 5 or 10 mg during a regimen of once-daily therapy, 24-hour urinary sodium and chloride outputs no longer differ from their postplacebo counterparts. Twenty-four-hour kaliuresis tends to increase in a dose-dependent fashion after the first dose of torasemide (torasemide 2.5 and 5 mg do not augment it significantly), but this tendency is no longer present after the seventh once-daily dose, when torasemide (2.5, 5, or 10 mg) does not elevate the mean 24-hour kaliuresis. Twenty-four-hour calciuresis tends to increase in a dose-dependent manner (torasemide 2.5 mg does not elevate it significantly) after the first dose of torasemide; this calciuretic effect does not change in intensity after 7 days of once-daily treatment. The time course of natriuresis over the 24 hours following the administration of any given formulation of a loop or of an early distal tubular diuretic to healthy subjects is alike after the first and after the nth once-daily dose; therefore, it constitutes a definite characteristic of any given oral formulation. In the case of torasemide, lower doses have more protracted effects on natriuresis, to the extent that the time course of natriuresis over the 24 hours after administration of torasemide 2.5 mg to healthy subjects resembles the time course after administration of hydrochlorothiazide 25 mg, rather than the time course after administration of the overtly diuretic formulation torasemide 10 mg.

Secretion of biliary calcium is increased in dogs with pigment gallstones.

We have previously demonstrated that gallbladder bile is supersaturated with calcium bilirubinate in a canine dietary model of pigment gallstones. Supersaturation resulted from combined increases in the concentrations of both biliary calcium and unconjugated bilirubin. The elevations in biliary calcium and unconjugated bilirubin concentrations remain unexplained but could possibly be due to increases in hepatic or ductular secretion, alterations in bile composition with respect to calcium-or bilirubin-binding affinity, decreases in absorption from the gallbladder lumen, or, in the case of unconjugated bilirubin, production within the lumen by hydrolysis of conjugated bilirubin. Here, we study a single possible cause for the observed increase in biliary calcium concentration during pigment gallstone formation in dogs. Secretion of calcium into bile in dogs with pigment gallstones before and after infusion of the bile salt, taurocholate, was compared to normal dogs. A significant increase in bile acid-independent bile flow and calcium output (CaO) was observed at any given bile acid output. Thus, plots of bile flow and CaO versus bile acid output yielded two separate functions in normal dogs and dogs with pigment gallstones. The slopes of these functions were similar, but intercepts extrapolated to zero bile acid output were markedly different, indicating that bile acid-independent, but not bile acid-dependent, bile flow and CaO was increased. The increase in CaO was not due to secretion of bile with increased concentrations of calcium but rather to the increases in the rate of bile flow. These findings might, in part, explain elevated calcium concentrations since increased amounts of calcium would be presented to the gallbladder in these animals during gallstone formation.

Human and experimental studies on renal eicosanoid response to long-term cadmium exposure

In order to assess the effects of long-term exposure to cadmium (Cd) on the renal metabolism of eicosanoids, the urinary excretion of 6-keto-prostaglandin F 1α (6-keto-PGF 1α), prostaglandin E 2 (PGE 2), prostaglandin F 2α (PGF 2α), and thromboxane B 2 (TXB 2) was determined in 37 workers exposed to Cd and in female Sprague-Dawley rats given 100 ppm Cd in drinking water for 10 months. Urinary output of sodium and calcium was also determined. The Cd-exposed workers showed an increased urinary concentration of 6-keto-PGF 1α, PGE 2, sodium, and calcium. The rise of 6-keto-PGF 1α was related to Cd levels in blood and weakly correlated with urinary sodium. Calcium in urine was not related to the concentration of the metal in blood and urine. A slight elevation in urinary TXB 2 was also observed in workers with blood Cd higher than 5 μg/liter. After 10 months of exposure to Cd, female Sprague-Dawley rats presented an enhanced urinary excretion of albumin, transferrin, β2-microglulin, sodium, and PGE 2 in urine. The latter was significantly correlated with albuminuria and transferrinuria. In conclusion the results show that chronic exposure to Cd induces changes in the urinary excretion of some eicosanoids. The possible relation of these changes to Cd-induced kidney dysfunction are discussed.

Calcium homeostasis in pregnant women receiving long-term magnesium sulfate therapy for preterm labor

The hypothesis of this study is that calcium homeostasis and bone mineralization are altered in pregnant women receiving long-term therapy with magnesium sulfate as compared with similar women not receiving magnesium sulfate to control preterm labor. Thirty-nine women between 24 and 32 weeks' gestation, matched for age, race, and duration of bed rest, were enrolled. Indices of calcium homeostasis in serum and urine were measured serially, and bone mineralization of the distal radius was measured at 1 and 11 weeks post partum. Magnesium therapy was administered for a mean duration of 26 +/- 14 days and a cumulative dose of 1405 +/- 963 gm. Serum concentrations of magnesium, phosphorus, and parathyroid hormone increased and those of calcium decreased from baseline values in the magnesium sulfate group and remained uniform throughout the 3-week investigation. The serum magnesium, phosphorus, parathyroid hormone, and calcium concentrations in the control group were unchanged during the study and differed significantly from those in the magnesium sulfate group (p < 0.001). Urinary output of magnesium, calcium, and copper was significantly greater in the magnesium sulfate group than in the control group throughout the study. Urinary losses of calcium in the magnesium sulfate group, approximately 800 to 900 mg/day, were substantial. Although radius bone density 1 week post partum did not differ between groups, the change in bone density from 1 to 11 weeks post partum was significantly lower in the magnesium sulfate group than in controls. These data suggest that calcium homeostasis is altered during and after long-term magnesium sulfate therapy. The marked, prolonged urinary calcium losses may affect maternal bone mineralization.

The influence of type of diet (roughage or concentrate) on the plasma level, renal excretion, and apparent digestibility of calcium and magnesium in resting and exercising horses

Summary In an experiment with six ponies, the effects of exercise and type of ration (roughage/concentrate) on the apparent digestibility, concentration in plasma (including the profile prior to feeding), and renal excretion of calcium and magnesium were studied. The ponies were fed twice daily with alfalfa hay or concentrate (15 g dry matter/kg body weight per day) supplemented with minerals; calcium intake was 278 or 312 mg/kg body weight per day for roughage and concentrate diets, respectively. For alfalfa hay and concentrate, the apparent total digestibility of calcium was 48.3 and 14.1%, and prececal digestibility (determined post mortem) 49.8 and 18.9%, respectively. Plasma levels of calcium were significantly different between ration types. They increased after feeding from 3.3 (roughage) and 2.8 mmol/l (concentrate) before feeding to maximal values of 3.7 mmol/12 hours after feeding roughage and 3.2 mmol/16 hours after feeding concentrate. The renal output of calcium after feeding followed the same pattern, total renal excretion amounted to 56% of total intake during roughage feeding and 19% during concentrate feeding. Plasma concentration and renal excretion of calcium were significantly reduced during exercise. The absorption, profile of concentration in plasma after feeding, and renal excretion of magnesium showed differences between diets similar to calcium; however, the concentration of magnesium in plasma was not affected by exercise. The glomerular filtration rate (inulin clearance) was reduced during exercise by 23% (concentrate) or 42% (roughage).