[Research on calcium pyrrolidinecarboxylate: comparative test with calcium chloride, calcium glutamate, calcium gluconate, calcium lactate and calcium levulinate].
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In 44 patients with congenital or acquired heart disease, functional class II--IV NYHAC, the effects of calcium gluconate (10 ml 10%) and calcium chloride (10 ml 5.5%) on hemodynamics, inotropy and myocardial oxygen consumption were investigated during and immediately after cardiosurgical procedures. There was a significant increase in blood pressure, left ventricular pressure, total systemic resistance, cardiac index, stroke index, peak dp/dt and myocardial oxygen consumption as well as in arterial perfusion pressure during extracorporeal circulation due to i.v.-injection of either one of the drugs. The positive inotropic effects were more pronounced after application of calcium chloride. In emergency situations during anaesthesia or resuscitation, therefore, calcium chloride seems to be of more advantage than calcium gluconate.
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The effects of commercially available calcium supplements (calcium carbonate, calcium gluconate, oyster shell preparation and bovine bone preparation) and gluconic acid on the absorption of calcium and magnesium were evaluated for 30 days in male Wistar rats. There were no differences in the apparent absorption ratio of calcium among rats fed each calcium supplement; however, the rats fed the calcium gluconate diet had a higher apparent absorption ratio of magnesium than the rats fed the other calcium supplements. Dietary gluconic acid also more markedly stimulated magnesium absorption than the calcium carbonate diet, and the bone (femur and tibia) magnesium contents of rats fed the gluconic acid diet were significantly higher than those of the rats fed the calcium carbonate diet. Furthermore, the weight of cecal tissue and the concentrations of acetic acid and butyric acid in cecal digesta of rats fed the calcium gluconate diet or the gluconic acid diet were significantly increased. We speculate that the stimulation of magnesium absorption in rats fed the calcium gluconate diet is a result of the gluconic acid component and the effect of gluconic acid on magnesium absorption probably results from cecal hypertrophy, magnesium solubility in the large intestine and the effects of volatile fatty acids on magnesium absorption.
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Calcium gluconate production by Aspergillus niger was investigated in shake flask, rolling shaker, air-lift reactor and stirred reactor. Growth pattern of the organism and fermentation conditions determined the yield of the product. High calcium gluconate production was achieved in air-lift reactor with pellet form of cell growth at moderate specific growth rate and biomass concentration. In another variation of air-lift reactor, when calcium carbonate was confined to a cellulose membrane, calcium gluconate production was maximum (149 g/L). At higher specific growth rate, obtained in shake flask, despite the formation of cell pellets, product formation was low. Physical separation of particulate calcium carbonate and growing cells favoured product formation. In stirred reactor pulpy mycelial growth was obtained and calcium gluconate production was poor.
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A strong calcium gluconate-producing strain of Aspergillus niger (MN181) was obtained by way of mutagenic treatment. Its growth was very slow with moderate sporulation. The strain was treated with N-methyl-N'nitro-N-nitrosoguanidine (MNNG) and some auxotrophic mutants were obtained. All were less productive than the parent strain in producing calcium gluconate. The reduced yield was corrected in the heterokaryons and diploids derived by crossing sister strains. One diploid strain (D4), heterozygous for auxotrophy and conidial colour markers was grown in the presence of 4% alcohol and 31 segregants were isolated which included both haploid and diploid strains. Their yields were studied and some recombinants were obtained which, in spite of the same yield of MN181, showed improvement in giving fast growth and abundant sporulation.
The effects of calcium gluconate on the utilization of magnesium and nephrocalcinosis in male Wistar rats made magnesium-deficient by adding excess dietary phosphorus (1.195 g of phosphorus/100 g of diet) and calcium (1.04 g of calcium/100 g of diet) were compared with the effects of calcium carbonate. The effects of dietary magnesium concentration on the magnesium status and nephrocalcinosis were also examined. Adding excess dietary phosphorus and calcium decreased the apparent magnesium absorption ratios and the concentrations of magnesium in the serum and femur and increased the deposition of calcium in the kidney, and the low magnesium condition (0.024 g of magnesium/100 g of diet) aggravated the deposition of calcium and the low magnesium status. The apparent magnesium absorption ratios and femur magnesium concentration in the rats fed a calcium gluconate diet (an equimolar mixture of calcium gluconate and calcium carbonate was used as a source of calcium) were significantly higher than in the rats fed a calcium carbonate diet (only calcium carbonate was used as a source of calcium), irrespective of dietary magnesium concentration. Dietary calcium gluconate lessened the accumulation of calcium in the kidney and increased the serum magnesium concentration compared with dietary calcium carbonate, when the rats were fed the normal magnesium diet (0.049 g of magnesium/100 g of diet) but not the low magnesium diet. We speculate that the increased utilization of magnesium by feeding the calcium gluconate diet to a limited extent prevented the low magnesium status and the severity of nephrocalcinosis caused by adding excess dietary phosphorus and calcium.
Cutaneous calcinosis following extravasation of calcium gluconate in a 6-day-old neonate is reported. After extravasation of a 10% calcium gluconate infusion, rapid and marked swelling, erythema, and signs of soft tissue necrosis developed over the dorsum of the right hand and wrist. Small eschars were soon formed on the skin surface and began to slough, the underlying base appearing necrotic. Through the small channels of the destroyed epidermis, tiny white pieces of calcific masses were eliminated spontaneously. Histologically, the dermal collagen was massively degenerated and the calcium deposits were found as amorphous masses throughout the dermis and subcutaneous adipose tissue, surrounded by mild lymphohistiocytic cell infiltration. This is a case which again warns of the danger of using 10% calcium gluconate intravenously in the neonate or young infant.
Calcium gluconate was administered to conscious horses at 3 different rates (0.1, 0.2, and 0.4 mg/kg/min for 15 minutes each). Serum calcium concentrations and parameters of cardiovascular function were evaluated. All 3 calcium administration rates caused marked increases in both ionized and total calcium concentrations, cardiac index, stroke index, and cardiac contractility (dP/dtmax). Mean arterial pressure and right atrial pressure were unchanged; heart rate decreased markedly during calcium administration. Ionized calcium concentration remained between 54% and 57% of total calcium concentration throughout the study. We conclude that calcium gluconate can safely be administered to conscious horses at 0.1 to 0.4 mg/kg/min and that administration will result in improved cardiac function.
Under hypercalcemia induced by calcium gluconate the degranulation of renomedullary interstitial cells accompanied with the increase in volume of the rough and smooth surfaced endoplasmic reticulum and enlargement of the Golgi apparatus were observed. The ultrastructural changes can be regarded as an expression of the increase of a synthetic and secretory activity of these cells. Because the changes of renomedullary cells observed in hypercalcemia induced by calcium gluconate are not really different from that observed in hypercalcemia induced by vitamin D3 (Roszkiewicz et al. 1979) it can suppose that these changes may be connected solely with a calcium serum elevation and that the renomedullary interstitial cells rather do not play any important role in vitamin D3 metabolism.
Topical therapy with 2.5% calcium gluconate gel is considered as the "first-aid" treatment of accidental hydrofluoric acid skin burns. The efficacy of three different gel formulations varying in the amount and/or nature of their gelling and moisturizing agents was experimentally evaluated. Thirty male Wistar-Han rats (250 g) were exposed to 60 mul of 40% hydrofluoric acid for 2 minutes on two spots (4 cm) of skin under pentobarbital anesthesia. One lesion was massaged with 1 g of gel (10 rats/type of gel) at 3 minutes; 30 minutes; 1 hour; 1 hour, 30 minutes; 2 hours; 3 hours; and 4 hours after injury. During the next 3 days, rats received a single daily application of gel. The other lesion for each rat remained untreated (control). From day 1 after injury to the end of the study (day 17), gel therapy reduced the number of extensive (-66%), severe (-44%), and moderate (-34%) lesions (P < .0001). It reduced (P < .001) the median Area Under the Curve day 0-17 of burn injury from 34.0 (25th to 75th percentile: 18.2-44.5; untreated lesions) to 17.7 (7.0-26.7); overall, there was three cases of treatment failure. At day 17, full wound recovery was obtained in 14 cases by gel therapy compared with 6 in the absence of treatment. The efficacy of the three gel formulations was comparable for all evaluated parameters. Repeated applications of a 2.5% calcium gluconate gel is an efficient treatment of experimental 40% hydrofluoric acid skin burn; few differences were observed between evaluated gel formulations.
The effect of calcium gluconate on the toxicity of the anthracycline antibiotic doxorubicin (DOX) in mice was studied. Calcium gluconate showed a significant protective action with respect to the DOX acute toxicity. When DOX was used in the lethal doses, up to the LD50s calcium gluconate protected all the mice from death. At the DOX LD100 or higher the antitoxic effect of calcium gluconate manifested itself in a lower death rate and/or in a higher lifespan of the animals (at least 2-fold). When DOX was used for the treatment course its chronic toxicity in the presence of calcium gluconate was 2 or more times lower by all the quantitative indices: the lifespan of the animals that died, the maximum and minimum total lethal doses of DOX, the latent period before the first mouse death, the overall duration of the DOX treatment course. The antitoxic effect of calcium gluconate also manifested itself in a lower DOX acute and chronic toxicity with respect to the gastrointestinal tract. Thus, calcium gluconate proved to be an effective DOX antitoxic modificator which provided the use of about 2 times higher single and courses doses of DOX in mice.