[The kinetic parameters of retainment and release of deposited in human tissue structures calcium].

The analysis of retainment and release kinetics of deposited in tissue structures calcium was made in the hypercalcemic conditions in 28 healthy volunteers (22 males and 6 females) of the age of 33 ± 6.5 years via drip infusion (Groups 1, 2) and in 9 individuals (3 males and 6 females) in 12 trials via stream infusion (Group 3). By the end of each hour after the termination of calcium infusion the amount of calcium retained in tissues was calculated (Mtis./kg); the parameters of its binding (specific buffer volume--ß3 sp, association constant--Ka, number of binding centers--n) were established using the Langmuir and Scetchard coordinates. The Group 1 volunteers (n = = 12) showed a section of positive cooperativity (a direct regression on Sketchard coordinates, Hill coefficient 3.36 ± 1.63) and 2 sections of the consecutive calcium separation from one set of noninteracting centers. 5 volunteers of Group 2 and 8 volunteers of Group 3 demonstrated a slight calcium delivery to tissues after 1 hour of observation which then followed for 2 volunteers of Group 2 and for 2 volunteers of Group 3. Other volunteers of Groups 2 and 3 showed a release of tissue-deposited calcium via the mechanism of the consecutive separation from one set of noninteracting centers with ßsp 3 times less and Ka 7 times higher than with the calcium infusion. The excretion of calcium in urine was the highest in Group 1 and the lowest in Group 3. The [Ca2+] and Mtis./kg values were normalized in Groups 1 and 2 the next morning and in Group 3 after 2-3 hours of observation. An assumption was made about the relationship between the tissue and kidney [Ca2+] normalizing mechanisms with hypercalcemia.

In vitro study of the antioxidative properties of the glucose derivatives against oxidation of plasma components

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Oxidative stress has been implicated in the pathogenesis of variety of diseases. Since the endogenous antioxidant defense may be not adequate to counteract the enhanced generation of oxidants, a growing interest in research for exogenous nutrients has been observed. The present study was designed to assess in vitro the antioxidative properties of the glucose derivatives: calciumD-glucarate, D-gluconic acid lactone, and sodium D-gluconate (0.5–3 mM) in the protection of plasma proteins and lipids, against the damage caused by 0.1 mM peroxynitrite (ONOO−). Exposure of plasma to ONOO− resulted in carbonyl groups increase, 3-nitrotyrosine (3-NT) formation, reduction in thiol groups, and enhanced lipid peroxidation. D-Gluconic acid lactone and sodium D-gluconate effectively decreased 3-NT formation; the antinitrative action of calcium D-glucarate was less effective. In plasma samples incubated with ONOO− and tested compounds, the level of carbonyl groups was decreased in comparison to plasma samples treated only with ONOO−. The level of protein −SH groups and glutathione was significantly higher in the presence of glucose derivatives than in plasma samples treated with ONOO− only. All the tested compounds had the inhibitory effect on the peroxynitrite-induced plasma lipids peroxidation. The results obtained from our work indicate that calcium D-glucarate, D-gluconic acid lactone, and sodium D-gluconate may partly protect plasma proteins and lipids against peroxynitrite-induced damages (AU)

Pharmacokinetics of calcium from calcium supplements in healthy volunteers.

Calcium supplementation is widely used in deficiency status and as an adjuvant in the treatment of osteoporosis. The objective of this study was to compare the oral bioavailability of calcium from tablets containing calcium fumarate to that of calcium gluconate. Twelve healthy volunteers participated in the study. Single-dose, two-treatment, two-sequence-crossover, randomized design test methodology was applied. The tablets were prepared by direct compression and were subjected to tests: drug content, hardness, friability, disintegration time and in vitro dissolution studies. The preparations were compared using pharmacokinetic parameters such as the area under the plasma concentration - time curve AUC((0-11)), peak plasma concentration C(max), time to reach maximum plasma concentration T(max). No statistically significant difference was observed for any of the parameters, and the 90% confidence intervals calculated for the ratio of the logarithmically transformed AUC((0-11)) values of both formulations were within the bioequivalence limit of 0.80-1.25. It can be concluded that the two tablet preparations of calcium are likely to be bioequivalent.

Dose-dependent characteristics of intravenous calcium therapy for hypocalcemic critically ill trauma patients receiving specialized nutritional support.

OBJECTIVE: The purpose of this investigation was to evaluate the dose-dependent characteristics of intravenous calcium gluconate therapy for hypocalcemic critically ill patients. METHODS: The dose-dependent characteristics of 2 g versus 4 g of intravenous calcium gluconate therapy were evaluated in 25 critically ill, adult multiple trauma patients with hypocalcemia. The calcium gluconate was infused at a rate of 1 g/h for both groups. Patients weighed within 90% to 120% of ideal body weight, had normal renal function, did not receive diuretic therapy, and did not have anasarca. RESULTS: Fifteen patients with mild hypocalcemia (serum ionized calcium concentration [iCa] 1-1.12 mmol/L) were given 2 g of calcium gluconate. Ten patients with moderate to severe hypocalcemia (iCa <1 mmol/L) were given 4 g. Each dosage group had a significant (P < or = 0.001) increase in iCa (from 1.07 +/- 0.05 to 1.17 +/- 0.05 mmol/L and from 0.92 +/- 0.08 to 1.16 +/- 0.11 mmol/L, respectively). Each dosage group retained about half of the dose in the exchangeable calcium space (P = NS between groups), but the higher dosage group retained significantly more elemental calcium overall (81 +/- 38 versus 201 +/- 50 mg, respectively, P < or = 001). Serum ionized calcium concentrations achieved a plateau without a further decline in iCa by 10 h after completion of the infusion for each dosage. CONCLUSION: About half of the administered elemental calcium dose was retained for each dosage group, with the higher dose (4 g) resulting in significantly more elemental calcium retention in the exchangeable calcium space. An iCa determination performed about > or =10 h after the completion of the calcium gluconate infusion should be sufficient time to ensure equilibration of iCa to assess the efficacy of the therapy. This mode of calcium therapy serves as an effective means for providing calcium to the acutely hypocalcemic, critically ill, multiple trauma patient.

An effective and better strategy for reducing body burden of radiostrontium.

In this study we have examined the effect of different calcium salts, Ca gluconate (CaG), Ca lactate (CaL), Ca carbonate (CaC) and Ca phosphate (CaP), on the clearance of radiostrontium (*Sr) administered either intraperitoneally (ip) (*Sr-ip group) or orally (*Sr-oral group) in rats. The influence of these Ca salts was examined in a group of animals administered *Sr ip, while the effect of three Ca salts (CaG, CaL and CaP) was studied in another group of rats given *Sr orally and compared with that of Ca alginate (CaA), normally advised for *Sr decorporation. Rats from both groups were subdivided into control and four experimental subgroups and were housed individually. The experimental subgroups were given the respective Ca salts (elemental Ca = 9 mg/rat/day) 2 h post 85Sr, and thereafter once daily. In the *Sr-ip group, CaG was administered ip while the other Ca salts were given orally. In the *Sr-oral group all Ca salts were administered orally. In addition, the diet of all the experimental subgroups was supplemented with the respective Ca salts to 2% elemental Ca. The whole-body retention (WBR) of *Sr in animals treated with Ca salts was found to be significantly reduced from 50-60% at 24 h to 20-30% at the end of 15 days compared with 70-80% at 24 h to 50-60% at the end of 15 days in the untreated control animals. The results strongly suggest that CaA could be replaced by any of the commonly used Ca salts for curtailing the WBR of *Sr. CaG which was administered ip, in the *Sr-ip group, was found to be more effective in reducing the WBR of *Sr.

Controlled study of citrate effects and response to i.v. calcium administration during allogeneic peripheral blood progenitor cell donation.

BACKGROUND: Leukapheresis procedures are generally performed at citrate anticoagulation rates extrapolated from shorter plateletpheresis procedures. However, neither the metabolic effects nor the management of associated symptoms have been critically evaluated during leukapheresis in healthy donors. STUDY DESIGN AND METHODS: Symptom assessments (n = 315) and laboratory analyses (n = 49) were performed during 244 procedures performed with and 71 without prophylactic calcium (Ca) chloride or Ca gluconate given at a dose linked to the citrate infusion rate (1.0-2.2 mg/kg/min). RESULTS: During leukapheresis of 12 to 25 L processed, ionized Ca and ionized magnesium (Mg) decreased as much as 35 and 56 percent, respectively, each exhibiting a tight negative correlation with marked increases in serum citrate levels. Significant increases in urinary Ca and Mg excretion accompanied the renal excretion of a large citrate load. Serum divalent cation levels remained depressed 24 hours after leukapheresis. Symptoms were more frequent in donors who were women, had low initial total Mg levels, and underwent procedures in which larger volumes were processed at higher citrate infusion rates. Ca infusions reduced clinically significant paresthesias by 96 percent and also attenuated decreases in serum potassium. Ca chloride maintained higher Ca levels than Ca gluconate. CONCLUSIONS: Prophylactic Ca infusions safely attenuate the marked metabolic effects of citrate administration and promote faster, more comfortable, leukapheresis procedures.

Solubility and intestinal transit time limit calcium absorption in rats.

Six-week-old male rats were placed on two high calcium regimens: one with calcium carbonate and monobasic calcium phosphate, with calcium content increased via calcium carbonate; and another with calcium phosphate and calcium gluconate, with calcium gluconate the source of increased calcium. Animals fed the gluconate-containing diets absorbed 29% of the ingested calcium over the entire calcium intake range, whereas those fed the calcium carbonate diets absorbed 25% over an intake range of 225 to 450 mg Ca/d, but at calcium intakes above 450 mg Ca/d their absorption reached a plateau at approximately 109 mg/d. Active calcium transport decreased with increased calcium intake in both the calcium carbonate- and calcium gluconate-fed groups. Nonsaturable transport was unchanged as a result of increasing calcium intake and did not differ among the diet groups. Because the absorptive processes were unaffected by the calcium source, events in the lumen must have been responsible for the observed differences. Because phosphate is nearly 18 times more soluble than carbonate, very little calcium of calcium carbonate origin can have been solubilized in the presence of phosphate and this, we conclude, accounts for the limit on calcium absorption observed in diets high in calcium carbonate. Moreover, when intake is expressed as soluble calcium, absorption approaches 50%, the value expected when intestinal transit time (approximately 3 h) is multiplied by 16%/h, the experimental value of nonsaturable absorption.

The effect of a standard oral calcium load given in two different forms on plasma ionized calcium and serum PTH.

A standard dose (1 g, 25.4 mmol) of calcium was administered both as calcium chloride in syrup and as Calcium-Sandoz Syrup (calcium glubionate and calcium galactogluconate) to 10 volunteers. Both dosage forms caused a significant rise in ionized calcium and a significant fall in concentration of serum PTH, the calcium chloride producing significantly greater changes. The urinary excretion of calcium measured over 5 h after calcium chloride was double that after Calcium-Sandoz. Calcium chloride, as expected, also gave rise to a decreased urine pH. Calcium chloride would be the better choice for an oral PTH suppression test.

Ionization and hemodynamic effects of calcium chloride and calcium gluconate in the absence of hepatic function.

Serial serum ionized calcium concentrations were measured before and after administration of either calcium chloride or calcium gluconate during the anhepatic stage of liver transplantation in 15 patients to determine the release of ionized calcium in the absence of hepatic function. When hypocalcemia (Ca++ less than 0.8 mM) occurred during the anhepatic stage, patients were randomly assigned to treatment with chemically equivalent doses of either calcium chloride (10 mg/kg, n = 8) or calcium gluconate (30 mg/kg, n = 7). Serum concentrations of ionized calcium and citrate, hematocrit, arterial blood gas tensions, acid-base state, and hemodynamic profiles were determined before and up to 10 min after calcium therapy. In both groups of patients initial similar and rapid increases in Ca++ (0.98 +/- 0.14 mM in the calcium chloride group and 1.05 +/- 0.10 mM in the calcium gluconate group) were followed by gradual decreases over the next 10 min. Measured hemodynamic values were similar in the two groups, and neither group showed improvement in cardiovascular function after calcium therapy, possibly because of the decrease in preload that occurred during the anhepatic stage. Equally rapid increases in Ca++ after administration of calcium chloride and gluconate in the anhepatic state suggest that calcium gluconate does not require hepatic metabolism for the release of Ca++ and is as effective as calcium chloride in treating ionic hypocalcemia in the absence of hepatic function.

[An analysis of calcium pidolate absorption and a comparison with that of a salt in common use, gluconate-lactate-carbonate, in postmenopausal osteoporosis]. / Análisis de la absorción del pidolato de calcio y comparación con la da una sal de uso común, el glucono-lactato-carbonato, en la osteoporosis postmenopáusica.

The absorption of calcium pidolate is studied in 10 females suffering from osteoporosis by oral overload compared to the results of the glucono-lactate-carbonate. 405 mq of Ca pidolate produced a higher excretion of calcium by urine and an increase of Ca levels in blood than that produced by 1000 mq of Ca glucono-lactate-carbonate. The tolerance and the lack of side effects were the common feature in both salts. There were no effects on parathyroid glands nor bone resorption. We concluded that calcium pidolate is a safe and efficient treatment for osteoporosis because of easy absorption, which is very helpful in maintaining the calcium balance.