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PubMed1999

Calcium absorption from the ingestion of coral-derived calcium by humans.

Recent dietary life involves frequent opportunities for the ingestion of purified, processed food products and preserved foods, and it has been pointed out that the current dietary mineral intake strongly tends toward nutritional imbalance. The Ryukyu Islands yield coral which contains calcium and magnesium in a content ratio of about 2 to 1, with their approximate contents of 20 and 10%, respectively. In this report, the calcium absorption from the ingestion of crackers into which the coral powder was incorporated (coral-added crackers) and that from ingestion of calcium carbonate-added crackers was comparatively assessed. Twelve healthy adult volunteers (6 men and 6 women) ingested coral-added crackers (calcium content: 525 mg) and calcium carbonate-added crackers (ditto) once each alternately on a cross-over design with a wash-out period of 3 d between the regimens. The study also included controls receiving neither cracker. The degree of intestinal absorption of calcium from coral-added crackers and that from calcium carbonate-added crackers was evaluated in terms of increment in urinary calcium excretion per dL of glomerular filtrate (GF) (difference between coral calcium and calcium carbonate) and increase in urinary calcium excretion per milligram creatinine (difference from control value). The increment in urinary calcium excretion per dL of GF during the latter half of the observation period after the ingestion of coral-added crackers was significantly greater than that during the latter half of the observation period after ingestion of calcium carbonate-added crackers (p = 0.039, paired t-test). A significant difference (from control value) in the increase of urinary calcium excretion per milligram creatinine was also observed (p = 0.0008). The present data, though from a relatively few study subjects, suggest that the calcium of coral origin is better absorbed from the intestine than calcium of calcium carbonate origin on the average.

Adult↗

PubMed2002

[Influence of calcium content among different calcium agents on absorbing and bone density of rats].

To identify the influence of different calcium contents among different calcium agents on absorbing and born density of rats, wistar rats are fed with diet containing different contents of calcium of different calcium agents. 3-day calcium metabolization experiment is carried out in the fourth week and atomic absorption spectrophotometry is applied to measure the calcium content of their dejecta and to estimate apparent absorptivity. Rats are killed in the twelfth week, and their thighbones are peeled. the results show that there is significant difference of the apparent absorptivity with different calcium intake. With the same content of calcium from nine kinds of calcium agents, the absorptivity is not significant different with an exception of those of active calcium, milk powder and oatmeal. Born density from the group of rats, which fed with diet with low level, middle level or high level of calcium, is obviously higher than that of rats fed with basic diet (P < 0.05). Born density of thighbone of the group of rats, which fed with diet with middle or high level of calcium content is not significantly different compared with that of rats fed with diet with calcium carbonate. The absorptivity of calcium is related with calcium content in diet. The effect of absorptivity of calcium agents tested is affirmative, but there is no difference of their effect in comparison with the calcium carbonate.

Animals↗

PubMed1984

Effects of dietary calcium on renal calcium, magnesium and phosphate excretion by the rabbit.

The renal handling of calcium, phosphate and magnesium was evaluated in rabbits fed diets varying in calcium content. Rabbits fed a low calcium diet (0.29%) exhibited a significant decrease in 24-hour excretion of calcium and in plasma calcium, and a significant increase in 24-hour excretion of phosphate, compared with rabbits fed a normal calcium diet (0.61%). Rabbits fed a high-calcium diet (1.89%) excreted significantly more calcium and less phosphate than the group fed normal dietary calcium. When measured under acute clearance conditions, the fractional excretion of calcium averaged 1-2% in rabbits fed either the low- or normal-calcium diets and increased to 6% in rabbits fed the high-calcium diet. In both acute and chronic studies, fractional phosphate excretion declined as the content of dietary calcium was raised. Magnesium excretion was not altered by the dietary calcium levels. Although calcium excretion by rabbits is set proportionately higher than that of other species, renal calcium handling in the rabbit is appropriate. Phosphate handling by the rabbit kidney similarly responds appropriately to dietary calcium manipulation.

Animals↗

PubMed1993

Localization and quantitation of calcium pools and calcium binding sites in cultured human keratinocytes.

Calcium plays a crucial role in regulating the growth and differentiation of cultured keratinocytes. However, the mechanism(s) of this regulation is not clear. Prior studies have shown that intracellular free calcium (Cai) increases with keratinocyte differentiation. In this study, in order to evaluate the role of cytosolic free calcium and organelle-bound calcium in keratinocyte differentiation, we quantitated and localized calcium pools in keratinocytes, utilizing the fluorescence probe indo-1 and ion-capture cytochemistry, respectively. Cai of undifferentiated keratinocytes was 80-120 nM, whereas Cai of differentiated keratinocytes was 200-300 nM depending on the extent of differentiation. The Cai of individual cells in an undifferentiated colony was heterogeneous (60-160 nM) with larger cells displaying higher Cai. Heterogeneity also was observed in the intracellular calcium-containing precipitates in the different layers of stratifying keratinocyte cultures using the cytochemical technique. Calcium precipitates were abundant in the lower cell layers, progressively decreasing apically, with the uppermost layer devoid of precipitates. Calcium-containing precipitates appeared as fine-to-coarse electron-dense granules on the plasma membrane, within the cytosol, mitochondria, nucleus, and vacuolar organelles. Whereas ionomycin in the presence of extracellular calcium increased the amount of intracellular calcium precipitates, EGTA removed calcium precipitates from organelles. Unlike intact epidermis, keratinocytes displayed no extracellular calcium reservoirs. Putative calcium binding sites, visualized by trivalent lanthanum (La) binding, were abundant on cell membranes and desmosomes of basaloid cells, but decreased in the upper cell layers. These studies revealed differences in the distribution of free ionic calcium (as determined by the fluorescence technique) and organelle-bound calcium (as determined by the cytochemical technique). Striking differences were also observed in calcium localization between intact epidermis and cultured epidermal cells. The localization pattern of calcium in cultured keratinocytes may reflect the hyperproliferative state of these cells, as in psoriatic epidermis, and/or the absence of a normal permeability barrier in these submerged cultures.

Binding Sites↗

PubMed1983

Calcium movements and intracellular calcium distribution in neoplastic GH3 cells.

Experiments were carried out to investigate the nature of the calcium homeostatic mechanisms in neoplastic GH3 rat pituitary cells. GH3 cells grown and maintained in Ham's F10 culture medium contained 35 nmoles calcium/mg cell protein. When stimulated by thyrotropin releasing hormone (TRH) or elevated K+ concentrations, only the latter caused cell calcium levels to rise although both resulted in hormone release. When exposed to EGTA, the GH3 cells lost calcium. When the temperature was lowered to 4 degrees C, the cells gained calcium and when rewarmed were able to extrude the previously accumulated calcium. The increased cell calcium following cold exposure could be blocked by prior treatment with rotenone. If rotenone was added subsequent to the cold exposure, it did not block the extrusion seen upon rewarming. In the absence of glucose in the medium, the GH3 cells took up more calcium upon exposure to 4 degrees C, and upon rewarming the cells could not return to their previous low levels. There are thus significant differences in calcium homeostasis between the neoplastic GH3 cells and their normal pituitary counterparts. When intracellular calcium was localized with the potassium pyroantimonate technique, there was calcium found in/on mitochondria, membrane bound vesicles and plasma membrane. Nuclear staining was sparse, and nucleolar staining was virtually absent. Upon stimulation with TRH, there was a decrease in mitochondrial calcium along with increases in both plasma membrane and nucleolar calcium levels. Since total calcium is unchanged, this indicates a significant calcium redistribution in response to TRH. The increased nucleolar calcium may reflect a calcium dependent increase in mRNA synthesis as has been reported. Since TRH presumably acts at a surface receptor, the increased plasma membrane calcium might be functionally related to receptor activation.

Animals↗

PubMed1981

Effects of casein and fibrin on calcium absorption and calcium homeostasis in the rat.

To test the hypothesis that individual proteins have specific effects on calcium absorption, two proteins, casein and fibrin, were pair-fed in diets to rats for 3 weeks. Each protein was fed at normal (1.2%) and low (0.02%) calcium intakes. Diets were matched in other nutrients. Calcium absorption, measured in vitro as serosal-to-mucosal concentration ratio of 45Ca developed by duodenal sacs, was the same for both protein groups when calcium intake was normal and was increased by both low-calcium diets. Comparing low-calcium diets, absorption was greater in fibrin-fed than casein-fed groups. Balance studies showed that casein- and fibrin-fed rats taking normal calcium diets excreted the same amounts of calcium and phosphorus in urine and feces. Fibrin-fed rats taking low calcium excreted twice as much calcium as casein-fed rats and had decreased serum calcium. The balance data suggest that, compared to casein, fibrin prevents absorption or promotes excretion of calcium when calcium intake is low, and the response to calcium depletion is enhanced calcium absorption. It is concluded that individual proteins can alter calcium transport through effects on overall calcium homeostasis.

Animals↗

PubMed1976

The effect of external calcium and lanthanum on platelet calcium content and on the release reaction.

Calcium compartments in calf platelets were studied using a lanthanum washout procedure to distinguish between surface-bound calcium and intracellular calcium. The calcium content of calf platelets ranges from 20 to 60 nmol/109. platelets and is sensitive to the calcium concentration of the suspending medium. With 1 mM calcium in the medium, calcium uptake is rapid and reaches steady state within 1-2 min. Results obtained with the lanthanum procedure indicate that it is the surface compartment which is most affected by the extracellular calcium concentration. The surface compartment appears to be saturable and is highly exchangeable. Although the total calcium as well as the calcium content of the surface and internal compartments are variable, the ratio of calcium in either compartment to the total saturated calcium is quite constant. The data indicate that 68-85% of the platelet calcium is located internally. Thrombin produces an immediate release of platelet calcium and labeled serotonin and an increase in the 45Ca2+ uptake of both the surface and internal compartments. The release reaction is not dependent upon exogenous calcium or an influx of exogenous calclium since it occurs even in the presence of ethyleneglycol-bis-(beta-aminoethylether)-N, N'-tetraacetic acid. Lanthanum, however, inhibits the release reaction possibly by blocking surface calcium site and reducing the mobility of endogenous platelet calcium.

Animals↗

PubMed1974

The response of the small intestine to vitamin D. Correlation between calcium-binding-protein production and increased calcium absorption.

1. The synthesis of calcium-binding protein, a protein produced in the small intestine in response to vitamin D, was investigated with a view to determining whether calcium-binding-protein production could be correlated with the stimulation of calcium absorption by vitamin D. 2. A radioimmunological assay, which can quantitatively estimate calcium-binding-protein concentrations as low as 1mug/g wet wt., was used to detect the synthesis of soluble calcium-binding protein. 3. When used on intestinal supernatants from chicks dosed with vitamin D, calcium-binding protein was not detectable at 8h but was present after 12h at a concentration of 8.6mug/g wet wt.; in agreement with this an increase in calcium absorption due to vitamin D was detected at 12h but not at 8h. 4. The synthesis of calcium-binding protein was also monitored directly by making use of the ability of the iodinated antiserum to bind specifically to nascent calcium-binding protein chains on intestinal polyribosomes; in this way calcium-binding-protein synthesis could be detected 8h after dosage with vitamin D. Further, the binding reaction indicated a near linear increase in the calcium-binding-protein-synthesizing capacity over a 16h period. 5. From the amount of calcium-binding protein present 12 and 24h after vitamin D administration it is calculated that calcium-binding-protein mRNA is produced at approx. 1mol/min per intestinal cell. 6. It is concluded that the high correlation between the initiation of calcium-binding-protein synthesis and the stimulation of calcium absorption by vitamin D strengthens the proposal that calcium-binding protein plays an important role in calcium transport.

Animals↗

PubMed2001

Calcium fortification of breakfast cereal enhances calcium absorption in children without affecting iron absorption.

OBJECTIVES: Provision of calcium-fortified foods may represent an important component of improving the calcium intake of children. We sought to determine whether the addition of calcium to cereal would have a net positive effect on calcium absorption without decreasing iron absorption. METHODS: Twenty-seven children, 6 to 9 years of age, were provided two servings per day (30 g of cereal per serving) of either a low (39 mg/serving) or fortified (156 mg/serving) calcium-containing cereal product for 14 days. Calcium absorption was measured by using stable isotopes added to milk (extrinsically labeled) and to the calcium-fortified cereal (intrinsically labeled). RESULTS: Fractional calcium absorption from the fortified cereal was virtually identical to that from milk. Fractional absorption of calcium from milk did not differ significantly when given with enriched or low-calcium-containing cereal. Total calcium absorption increased from 215 +/- 45 mg/d to 269 +/- 45 mg/d with the addition of the calcium-fortified cereal (P <.001). Iron absorption was similar when children received the calcium-fortified cereal or unfortified cereal. CONCLUSIONS: The addition of a moderate amount of calcium to a cereal product was beneficial to calcium absorption and did not interfere with iron absorption. Use of calcium-fortified food products may be considered a practical approach to increasing the calcium intake of children.

Absorption↗

PubMed1992

Calcium regulating hormones after oral and intravenous calcium administration.

The aim of this study was to determine the changes in serum calcium concentration and in the concentrations of calcium regulating hormones after a single oral or intravenous calcium administration. Standard dosages of calcium, as used in routine patient care, were employed. Intact parathyrin, calcitonin, calcitriol, calcidiol, total calcium, ionized calcium, total protein and phosphate were determined in 12 healthy young men before and up to 8 h after oral and intravenous administration of calcium. During a fortnight there were four study days with 1000 mg calcium orally (p.o.), 2000 mg orally, 180 mg calcium intravenous (i.v.) and a control day without calcium. During the study the men were on a low calcium diet. We observed a sharp increase in the calcium concentration after i.v. administration (15 min: total Ca: + 0.48 +/- 0.32 mmol/l; ionized Ca: + 0.25 +/- 0.15 mmol/l; p < 0.01). The concentration increase after the two oral loads was nearly identical. The maximal concentration of total calcium was reached after 120 min (1000 mg: + 0.1 +/- 0.04 mmol/l; p < 0.001; 2000 mg: + 0.12 +/- 0.04 mmol/l; p < 0.001). There was a significant increase in urinary calcium after all modes of calcium administration. Calcitonin increased significantly only after i.v. injection of calcium (+ 9.2 +/- 3.4 pmol/l; p < 0.001) while parathyrin decreased significantly after all modes of calcium administration (i.v.: 15 min: -1.9 +/- 0.88 pmol/l; p < 0.01; 1000 mg: 90 min: -0.78 +/- 0.75 pmol/l; p < 0.001; 2000 mg: 90 min: -1.02 +/- 0.57 pmol/l; p < 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

Administration, Oral↗

PubMed1982

The effect of calcium load on the calcium permeability of sarcoplasmic reticulum.

The effect of intravesicular and extravesicular calcium concentration on the passive efflux from sarcoplasmic reticulum (SR) vesicles isolated from cardiac and skeletal muscle was determined by measuring net efflux of calcium after stopping pump-mediated fluxes. The apparent permeability, calculated as the passive efflux divided by the total intravesicular calcium, depended on calcium load. This dependence of the apparent permeability on calcium load could be explained by the presence of intravesicular calcium-binding sites with a dissociation constant less than 10(-3) M. When the intravesicular bound calcium was taken into account, passive calcium efflux was found to be linearly related to the difference in calcium concentration across the SR membrane. Thus the permeability of the SR membrane is independent of intravesicular and extravesicular calcium concentration in the ranges investigated. The average first order rate constant for passive calcium efflux for six preparations was 0.8 +/- 0.2 min-1 for skeletal and 0.7 +/- 0.1 min-1 for cardiac SR. The amount of intravesicular bound calcium for the same preparations was 33 +/- 6 nmol mg-1 for skeletal and 13 +/- 2 nmol mg-1 for cardiac SR. The first order rate constants were unaffected by Mg concentration between 0.1 +/- 15.1 mM and by the presence of an ATP-regenerating system. The results suggest that some minimal calcium load may be required in order to observe a substantial passive calcium efflux, the passive calcium efflux is not carrier mediated, and passive calcium efflux is not a likely route of calcium release during excitation-contraction coupling.

Animals↗

PubMed2006

A nonadherent cell-based HTS assay for N-type calcium channel using calcium 3 dye.

The N-type calcium channel is a member of the voltage-sensitive calcium channel family and plays a major role in the regulation of neurotransmitter release in the central and peripheral nervous systems. Inhibition of the N-type calcium channel by intrathecal administration of the channel-specific blocker omega-conotoxin MVIIA (ziconotide) is efficacious in the treatment of severe chronic pain. While no orally active small molecules that block the N-type calcium channel are currently available, the discovery of such potentially valuable therapeutics would benefit from a reliable, high throughput assay. However, the assay of N-type calcium channel activity by measuring calcium influx using nonadherent cells in a high throughput fashion has not been achieved before, likely owing to a number of technical hurdles. For example, the measurement of calcium levels in nonadherent cells using conventional calcium indicators, such as Fluo-3 or Fluo-4, requires dyeloading the cells in suspension and subsequent removal of extracellular dye. This limits plate throughput and requires constant handling of the cells. To assay the N-type calcium channel activity using a nonadherent cell line in a high throughput manner, we investigated the application of no-wash calcium assay kits from Molecular Devices Corp. (Sunnyvale, CA): FLIPR Calcium, FLIPR Calcium Plus, and FLIPR Calcium 3. We show here that the FLIPR Calcium 3 assay kit can be used with nonadherent IMR-32 cells to measure potassium-evoked, omega-conotoxin MVIIA-reversible calcium flux with high throughput (15,000 data points/day), high quality (Z approximately 0.6), and minimal handling of the cells. Thus, this assay can be used to reliably and efficiently screen large compound libraries in the search for small molecule N-type calcium channel blockers.

Calcium↗

PubMed1999

Effect of histamine H2-receptor antagonist on the phosphorus-binding abilities of calcium carbonate and calcium lactate in hemodialysis patients.

The effect of histamine H2-receptor antagonist (famotidine) on the phosphorus-binding abilities of calcium carbonate and calcium lactate were examined in 13 chronic hemodialysis patients. In seven patients receiving calcium carbonate, famotidine (20 mg/d) was given because of gastroduodenal disorders, and calcium carbonate was replaced with calcium lactate as a phosphorus binder after 4 wk of treatment with famotidine. With the 4-wk administration of famotidine accompanied by calcium carbonate, the serum phosphorus level increased from 6.3+/-0.9 to 7.1+/-0.5 mg/dl (P<0.05). However, with the substitution of calcium lactate, the serum phosphorus level decreased significantly when compared to that before substitution (6.3+/-0.2 and 6.0+/-0.9 mg/dl after 4 and 8 wk of substitution, respectively), despite continued administration of famotidine. Serum calcium, creatinine, alkaline phosphatase, high sensitive parathyroid hormone, blood urea nitrogen, arterial blood pH, and bicarbonate were not significantly altered during the trial period. In six control patients treated with calcium carbonate alone, there were no statistical changes in serum calcium and phosphorus levels after substitution of calcium lactate for calcium carbonate. These results suggest that famotidine significantly affects the phosphorus-binding ability of calcium carbonate, but not that of calcium lactate. A careful observation of changes in the serum phosphorus level should be required in hemodialysis patients receiving calcium carbonate and histamine H2-receptor antagonists. Calcium lactate may be useful as a phosphorus binder in such hemodialysis patients.

Adult↗

PubMed1986

Calcium metabolism, renin activity, and the antihypertensive effects of calcium channel blockade.

Although abnormalities of calcium metabolism have been described in various hypertensive states, the specific manner in which these abnormalities contribute to the increased pressure remains unclear. Our own group, in attempting to resolve the seemingly contradictory evidence thus far obtained, has adopted an approach emphasizing the clinical as well as biochemical heterogeneity among hypertensive subjects. We have observed the following: broad-based deviations of calcium ionic and hormonal indices in patients with essential hypertension; these deviations are linked with concurrent deviations in the renin-aldosterone system. Thus, low-renin subjects exhibit a calcium ionic and hormonal profile suggestive of calcium deficiency, whereas high-renin subjects have an opposite metabolic profile suggestive of calcium excess; blood pressure responses to dietary salt loading may also differ among renin subgroups of essential hypertension and may be mediated by salt-induced alterations of calcium metabolism. In the absence of these alterations, dietary salt intake results in little or no change in blood pressure; and calcium as a dietary supplement may itself possess antihypertensive properties in targeted subgroups of essential hypertensive patients, preferentially in low-renin, lower ionized calcium subjects. Interestingly, calcium channel blockade also preferentially lowers pressure in low-renin, lower serum ionized calcium forms of hypertension and may define those subjects whose elevated pressure is most dependent on extracellular calcium. Conversely, renin profiling or serum ionized calcium measurements may be used clinically to help target subjects most likely to benefit from calcium channel antagonists. Lastly, unlike other antihypertensive drug classes, high salt intake does not blunt, and may even enhance, the hypotensive effects of calcium channel blockade, lessening the need for stringent dietary recommendations. Altogether, these heterogeneous alterations of calcium metabolism in essential hypertension suggest that the linkage between the regulation of calcium metabolism, renin system activity, and blood pressure in essential hypertension is of pathophysiologic as well as therapeutic relevance.

Blood Pressure↗

PubMed1990

Effects of supplemental dietary calcium on the intestinal association of calcium, phosphate, and bile acids.

It has been suggested that supplemental dietary calcium decreases hyperproliferation of colonic epithelial cells because calcium precipitates and thus inactivates luminal bile acids. Therefore, 12 healthy men were studied before and after dietary calcium supplementation (35.5 mmol/day) to quantify intestinal associations of calcium, phosphate, and bile acids. The supplemental dietary calcium was almost completely (95%) recovered, mainly in feces. Calcium increased the fecal excretion of both phosphate (31%) and bile acids (53%) and decreased the ratio of dihydroxy to trihydroxy bile acids in duodenal bile almost twofold. In vitro studies showed that precipitation of glycodeoxycholic acid was caused by the formation of insoluble calcium phosphate. Water-soluble and calcium-associated amounts of phosphate and bile acids in feces were measured by resolubilization studies, using the calcium chelator ethylenediaminetetraacetate. In both the control and calcium periods, significant amounts of phosphate (80% and 90%) and bile acids (33% and 50%) were calcium-associated. Moreover, the calcium-induced increments in fecal phosphate and bile acids were completely calcium-associated. Calcium decreased the amount of water-soluble phosphate but not of bile acids. These results indicate that supplemental calcium stimulates formation of insoluble calcium phosphate in the intestinal lumen and thus increases binding of luminal bile acids.

Bile Acids and Salts↗

PubMed1993

Characterization of the inositol trisphosphate-sensitive and insensitive calcium stores by selective inhibition of the endoplasmic reticulum-type calcium pump isoforms in isolated platelet membrane vesicles.

In mixed platelet membrane vesicles the presence of two distinct endoplasmic reticulum-type calcium pump enzymes of 100 and 97 kD molecular mass has been demonstrated. We have previously shown that both calcium pumps were recognized by polyclonal anti-sarcoplasmic reticulum calcium pump antisera [11]. In the present work we studied the effects of several calcium pump inhibitors on active calcium transport and inositol trisphosphate-induced calcium release in these vesicles in an attempt to assign the two calcium pump isoenzymes to specific calcium pools. The effect of the PL/IM 430 inhibitory anti-calcium pump antibody was compared to that of other calcium pump inhibitors acting predominantly on the 100 and the 97 kD calcium pump isoforms, respectively. The PL/IM 430 antibody, which recognized the 97 kD pump on Western blots and 2,5-di-(tert-butyl)-1,4-benzohydroquinone, which inhibited phosphoenzyme formation of the same pump isoform, inhibited calcium accumulation predominantly into an inositol trisphosphate-releasable calcium pool. On the other hand, low concentration of thapsigargin, which inhibited phosphoenzyme formation mainly of the 100 kD pump isozyme, had a more pronounced effect on calcium uptake into an inositol trisphosphate-resistant pool. These data suggest that in platelets the 97 kD calcium pump isoform is likely to be associated with the inositol trisphosphate-sensitive calcium storage organelle.

Antibodies, Monoclonal↗

PubMed1985

Cold ischemic arrest: comparison of calcium-free and calcium-containing solutions.

Isolated pumping rat hearts, perfused with reconstituted blood, were studied to compare the effects of 30 minutes of ischemic arrest following calcium-free or normal, calcium-containing cold cardioplegia on recovery of mechanical function, lactate production, myocardial adenosine triphosphate concentration, and release of creatine kinase (CK). As in clinical situations, the volume of the infusate was only three to four times the intracavitary blood volume. Hearts arrested with calcium-free solution showed incomplete recovery of mechanical function, whereas hearts arrested with calcium-containing solution recovered completely. After calcium-free arrest, stroke volume recovered to 76 +/- 29% (standard deviation [SD]) of its prearrest value. Enzyme release (CK) was significantly higher after calcium-free cardioplegia (7.7 +/- 4.6 units [SD]) than after cardioplegia with normal calcium (2.1 +/- 1.6 units [SD]). Since the addition of only 0.025 mmol calcium ions to a liter of calcium-free solution completely prevented its negative effect, it was concluded that calcium-free cardioplegia may cause limited but pronounced damage to myocardial cells, presumably because it removes calcium from the cellular membranes--the so-called calcium paradox. Probably due to residual calcium in blood and extracellular fluid, the damage is not so extensive after calcium-free cardioplegia as to be noticeable in clinical surgical situations. Residual calcium in the heart does not exclude the possibility, however, that a calcium paradox occurs in small scattered areas of the heart.

Adenosine Triphosphate↗

PubMed1998

Randomized crossover study comparing the phosphate-binding efficacy of calcium ketoglutarate versus calcium carbonate in patients on chronic hemodialysis.

The objective of the study was to evaluate the phosphate-binding efficacy, side effects, and cost of therapy of calcium ketoglutarate granulate as compared with calcium carbonate tablets in patients on chronic hemodialysis. The study design used was a randomized, crossover open trial, and the main outcome measurements were plasma ionized calcium levels, plasma phosphate levels, plasma intact parathyroid hormone (PTH) levels, requirements for supplemental aluminum-aminoacetate therapy, patient tolerance, and cost of therapy. Nineteen patients on chronic hemodialysis were treated with a dialysate calcium concentration of 1.25 mmol/L and a fixed alfacalcidol dose for at least 2 months. All had previously tolerated therapy with calcium carbonate. Of the 19 patients included, 10 completed both treatment arms. After 12 weeks of therapy, the mean (+/-SEM) plasma ionized calcium level was significantly lower in the ketoglutarate arm compared with the calcium carbonate arm (4.8+/-0.1 mg/dL v 5.2+/-0.1 mg/dL; P = 0.004), whereas the mean plasma phosphate (4.5+/-0.3 mg/dL v 5.1+/-0.1 mg/dL) and PTH levels (266+/-125 pg/mL v 301+/-148 pg/mL) did not differ significantly between the two treatment arms. Supplemental aluminum-aminoacetate was not required during calcium ketoglutarate treatment, while two patients needed this supplement when treated with calcium carbonate. Five of 17 (29%) patients were withdrawn from calcium ketoglutarate therapy within 1 to 2 weeks due to intolerance (anorexia, vomiting, diarrhea, general uneasiness), whereas the remaining 12 patients did not experience any side effects at all. The five patients with calcium ketoglutarate intolerance all had pre-existing gastrointestinal symptoms; four of them had received treatment with cimetidine or omeprazol before inclusion into the study. Calculations based on median doses after 12 weeks showed that the cost of the therapy in Denmark was 10 times higher for calcium ketoglutarate compared with calcium carbonate (US$6.00/d v US$0.65/d). Calcium ketoglutarate may be an effective and safe alternative to treatment with aluminum-containing phosphate binders in patients on hemodialysis who are intolerant of calcium carbonate or acetate because of hypercalcemia. However, care must be exercised when dealing with patients with pre-existing gastrointestinal discomfort. Due to the high cost of the therapy, calcium ketoglutarate should be used only for selected patients.

Adult↗