[Research on calcium pyrrolidinecarboxylate: comparative test with calcium chloride, calcium glutamate, calcium gluconate, calcium lactate and calcium levulinate].
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A randomized prospective study in both children and dogs compared ionization of calcium chloride and calcium gluconate. Five conditioned dogs under halothane anesthesia received calcium chloride (4, 8, 12 mg/kg) and calcium gluconate (14, 28, 42 mg/kg) intravenously. Ten children scheduled for burn wound excision and grafting received both calcium chloride (2.5 mg/kg) and calcium gluconate (7.5 mg/kg) injected through a central venous cannula. Ionized calcium was measured at 0, 0.5, 1, 3, 5, and 10 min in the children, and 0, 0.5, 1, 2, 3, 4, 5, 10, 20, and 45 min in the dogs. The authors conclude that equal elemental calcium doses of calcium gluconate (10%) and calcium chloride (10%) (approximately 3:1), injected over the same period of time, are equivalent in their ability to raise [Ca++] during normocalcemic states in children and dogs; the changes in [Ca++] following calcium administration are short-lived (minutes); rapidity of ionization seems to exclude hepatic metabolism as an important factor in the dissociation of calcium gluconate; and equivalent rises in [Ca++] produced by calcium gluconate or calcium chloride resulted in equivalent cardiovascular effects. The authors feel that either form of calcium salt would be satisfactory if indicated during cardiopulmonary resuscitation or for the treatment of ionized hypocalcemia due to massive blood transfusion.
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.
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The effects of calcium chloride on glandular stomach carcinogenesis induced by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) and sodium chloride were investigated in male outbred Wistar rats. Animals were given MNNG solution (100 p.p.m.) as drinking water and simultaneously fed a diet supplemented with 5% sodium chloride for 8 weeks. Matched negative controls received neither MNNG nor sodium chloride. Rats were then fed basal diet and given calcium chloride solution (1 or 0.2%) or tap water for the following 52 weeks. The incidences and multiplicities of preneoplastic hyperplasias in the glandular stomachs of rats given MNNG/sodium chloride followed by 1 and 0.2% calcium chloride were significantly lower than those in rats given MNNG/sodium chloride alone. The inhibitory effects of calcium were exerted in a dose-dependent manner. Calcium treatment also showed a tendency to inhibit the development of gastric adenocarcinomas although this was not statistically significant. Rats without carcinogen treatment had neither carcinomas nor preneoplastic hyperplasias in the glandular stomach. Calcium intake also significantly reduced the levels of malondialdehyde, a measure of lipid peroxidation, in the gastric mucosa and urine, the former in a dose-dependent manner. Thus, calcium chloride exerted inhibitory effects when given during the post-initiation phase of two-stage glandular stomach carcinogenesis in rats.
Calcium chloride increased the liver insulinase activity (LIA) in normal rabbits. No significant changes were noted in the plasma insulinlike activity (PILA), serum zinc level (SZ), and pancreatic zinc content (PZ). Insulin elevated PILA, SZ and PZ but did not affect LIA. Calcium chloride enhanced the effect of insulin on PILA, SZ and PZ. However, insulin did not affect the action of calcium chloride on LIA. Tolbutamide raised PILA, inhibited both LIA and SZ but did not affect PZ. Calcium chloride produced no change in the action of tolbutamide on PILA. On the other hand, tolbutamide prevented the rise of PILA obtained by calcium chloride. PZ was unaltered with calcium chloride and tolbutamide combination. Phenformin increased PILA, LIA, SZ and PZ. When it was given with calcium chloride no further changes in PILA and PZ were observed. The elevation of SZ was abolished but the rise of LIA was synergized. In alloxanized rabbits, LIA was decreased by calcium chloride. No changes were found in PILA, SZ and PZ. Insulin elevated PILA, LIA and SZ although it reduced PZ. Calcium chloride stimulated insulin effect on PILA, did not affect its action on SZ or PZ, and antagonized its effect on LIA. Tolbutamide increased LIA and SZ but did not affect PILA or PZ. Calcium chloride could not change the effect of tolbutamide on SZ or PILA although it could abolish the action of this drug on LIA and PZ. Phenformin significantly lowered PILA, LIA and PZ but raised SZ. Calcium chloride combination with phenformin produced a further decrease in LIA but no other changes in PIAL, SZ or PZ were recorded.
The effectiveness of calcium chloride in asystole has been challenged; retrospective studies have not supported its use. We conducted a prospective, randomized, blinded study comparing the effectiveness of calcium chloride with saline in the prehospital paramedic setting. Seventy-three patients who had received epinephrine, bicarbonate, and atropine and were in refractory asystole were included in the study, which was conducted from October 1982 to October 1983. Traumatic and pediatric arrests were excluded. The successful resuscitation rate was three of 39 in the calcium group versus one of 34 in the saline group (P less than .37). A successful resuscitation was defined as the conveyance of a patient with a pulse and a rhythm to an emergency department. Groups were analyzed for sex, age, and witnessed arrests. There was no statistically significant difference between the groups. No patient who was resuscitated successfully in the field was discharged from the hospital alive. We conclude that calcium chloride is not of value in resuscitating patients from refractory asystole in the prehospital cardiac arrest setting.
The denaturations of ribonuclease A by calcium chloride and lithium chloride were studied by circular dichroism measurements in the far-ultraviolet region. The temperature dependence of the equilibrium constant for the unfolding of the protein by calcium chloride and lithium chloride gave values of 46 and 52 kcal mol-1 (1 cal = 4.1868 J) for the enthalpy of denaturation at 25 degrees C and pH 7.0, respectively. Thermodynamic parameters for the denaturation by calcium chloride and lithium chloride are compared with those for the heat and guanidine hydrochloride denaturation. It has been observed that the thermodynamic quantity, be it free energy, entropy, or enthalpy, cannot be related quantitatively to the extent of unfolding measured by various conformational properties of the protein.
The effects of oral administration of calcium chloride solutions to dairy cows were studied. When a 0.3 per cent solution was given ad libitum, and as the sole source of water for a period of 75 days, we observed no significant changes in feed consumption, body weight or milk production. The average daily water intake was increased by approximately 20 per cent, and signs of slight gastro-intestinal irritation were seen. No major changes in blood hemoglobin levels, hematocrits, total and differential white cell counts or thrombocyte numbers could be attributed to the treatment. We observed no significant effect on the serum calcium, chloride, magnesium, potassium, or sodium content. The level of inorganic phosphate in the serum rose to higher, but still normal values. During the entire experiment the urine pH was abnormally acid for dairy cows. Electrocardiograms were taken after 45 days of calcium chloride administration, and they appeared normal. When 0.1 and 0.2 per cent solutions were given as the sole source of water for a period of 81 days, the cows remained in good condition, and we observed no changes in appetite, body weight or milk production. In general, dairy cows will refuse to drink calcium chloride solutions when the concentration exceeds 0.5 per cent, even when they have been deprived of water for 18-24 hours. On the other hand, since the administration of lower concentrations for periods of 75 and 81 days did not cause any clinical sign of disease, it seems that on farms where more than one source of water are usually available, poisoning of dairy cattle by calcium chloride in solution is quite unlikely.
Sodium, potassium, chloride, calcium, inorganic phosphorus (Pi) and magnesium contents in the serum of 75 myocardiopathic chagasic patients together with that in 29 healthy controls were determined. Blood samples were taken by catheterization from the superior cava vein (SCV), coronary sinus (CS), pulmonary artery (PA) and a peripheral artery, usually the femoral (FA). The results show that the average serum sodium, potassium, chloride, calcium and PI were invariably different in most samples, except the levels of potassium in SCV and Pi levels in FA. The serum concentration of magnesium was significantly different only in the blood of CS. In general one can observe that in the chagasic patients the serum sodium, chloride and calcium tend to diminish while serum potassium, Pi and magnesium tend to increase, especially in CS blood. The coronary gradient indicates that sodium, chloride and calcium tend to deposit in heart tissues, whereas the other elements (potassium, magnesium and Pi) tend to be released from this tissue. The systemic and peripheric gradients suggest that the chemical elements under study tend either to deposit in/or be released from different tissues depending on the course of development of the chagasic myocardiopathy.
Ultrastructural changes of the parathyroid glands of 18-day-old mouse fetuses after administration of calcium chloride (calcium) or ethylenediaminetetraacetic acid (EDTA) were examined. Many chief cells in the parathyroid glans of the calcium-treated mouse fetuses contained poorly developed Golgi complexes and cisternae of the granular endoplasmic reticulum and many secretory granules as compared with those of the control fetuses. Many chief cells in the glands of the EDTA-treated mouse fetuses contained well-developed Golgi complexes and cisternae of the granular endoplasmic reticulum and many prosecretory granules as compared with those of the control fetuses. These findings suggest that calcium or EDTA affects the secretory activity of the parathyroid gland of the mouse fetus.
In 30 dogs on right heart bypass we compared the effects of isoproterenol with those of calcium chloride on myocardial oxygen consumption and on left ventricular function in the setting of ventricular depression produced by ionized hypocalcemia. In 22 dogs (Groups A and B) either isoproterenol or calcium chloride was infused, left ventricular function curves were generated, and end-diastolic pressure vs segment length plots were obtained. In 8 dogs (Group C), with initial hypocalcemia, both isoproterenol and calcium chloride were infused separately in random order to produce an equal decrease in left ventricular end-diastolic pressure at constant mean aortic pressure, heart rate, and cardiac output. Myocardial oxygen consumption and indices of left ventricular function were obtained. In Groups A and B, both drugs, when administered to the ventricle depressed by hypocalcemia, displaced left ventricular function curves upward and to the left. Left ventricular stroke work at constant left ventricular end-diastolic pressure increased (from 13.0 +/- 1.3 to 31.2 +/- 2.3 g X m for isoproterenol; from 13.9 +/- 2.5 to 32.5 +/- 2.5 g X m for calcium chloride). In Group C, there were no significant differences between left ventricular end-diastolic pressure, end-diastolic internal diameter, myocardial oxygen consumption, or peak left ventricular dP/dt in the hypocalcemic periods preceding isoproterenol and calcium chloride infusion. When the two drugs caused matched decreases in left ventricular end-diastolic pressure (-7.4 +/- 0.5 cm H2O for isoproterenol; -7.3 +/- 0.8 cm H2O for calcium chloride) there were similar decreases in end-diastolic internal diameter. However, isoproterenol was associated with a significantly greater (P less than 0.001) myocardial oxygen consumption (13.7 +/- 0.4 ml X 100 g-1 X min-1) than calcium chloride infusion (11.9 +/- 0.4 ml X 100 g-1 X min-1), as well as a greater peak left ventricular dP/dt (P less than 0.005).
The effectiveness of calcium in electromechanical dissociation (EMD) has been challenged. Retrospective studies have been contradictory. To determine its effectiveness a prospective, randomized, blinded study comparing calcium chloride and saline in refractory EMD was carried out in the pre-hospital setting from October 1982 to October 1983. Only patients who had received epinephrine and bicarbonate and were refractory were entered in the study. All trauma and pediatric arrests were excluded. Ninety patients presented in refractory EMD. Overall, eight of 48 who received calcium were resuscitated successfully in the field; two of 42 who received saline were resuscitated successfully (P less than .07). A successful resuscitation was defined as the conveyance of a patient with a pulse and a rhythm to an emergency department. Patients were analyzed for age, sex, and witnessing of arrest. There was no statistical difference in demographic data. When the group of EMD patients was broken down into subgroups based on the width of QRS, it was noted that patients with a QRS width less than 0.12 did not respond to calcium, whereas the successfully resuscitated in the group with widened QRS or ischemic changes (N = 70) was eight of 39, compared with one of 31 not receiving calcium (P less than .028). Only one patient who was resuscitated successfully was discharged from the hospital alive. Calcium has been shown to be effective in the cardiac resuscitation of patients in refractory EMD. There may be a subset of patients with widened QRS complexes or ischemic changes who will benefit to a greater extent from the use of calcium chloride.
Partial molar heat capacities (CP2 degrees) and volumes (V2 degrees) for some amino acids and peptides were measured in 1 M aqueous calcium chloride solutions at 298.15 degrees K using a Picker flow microcalorimeter and an oscillating-tube digital density meter. Using the data for these amino acids and peptides in water, the corresponding partial molar heat capacities of transfer (CP2,tr degree) and volumes (V2,tr degree) from water to 1 M aqueous calcium chloride were deduced. These thermodynamic parameters are significantly positive, indicating that strong interactions occur between the ions of calcium chloride and the charged centres of these amino acids and peptides. A comparison has been made with a similar transfer of these compounds to sodium chloride solutions. The thermodynamic parameters of the transfer of peptide group (-CONH) are much more positive in calcium chloride than in sodium chloride solutions. The implication of this result for the ability of calcium chloride to act as a stronger destabilizer of protein conformation is discussed.
While calcium administration has been recommended in CPR, its beneficial effects have been challenged. The effectiveness of calcium chloride was evaluated and compared with epinephrine during successive episodes of electromechanical dissociation (EMD) after ventricular fibrillation in closed-chest dogs. Each of three successive episodes of CPR was randomly and blindly treated by repeated (every 2 min) injections of 5 ml H2O plus either 500 mg of calcium chloride (CaCl2), 1 mg of epinephrine (Epi), or 5% dextrose (D5W). Of 42 CPR attempts performed on 16 dogs, 16 were reversed by only chest compression and artificial ventilation. For the 26 CPR with pharmacologic intervention, recovery was obtained after one injection in 5 of 6 Epi but only in 4 of 11 CaCl2 and 4 of 9 D5W. Only four CPR attempts were ultimately unsuccessful, all in CaCl2 group. During recovery, the Epi group showed significantly higher arterial pressures and heart rates but less severe acidemia. In this model, calcium chloride alone is ineffective during EMD.
Magnesium sulfate worsens maternal hypotension and fetal oxygenation during hemorrhage in gravid ewes. The purpose of this study was to determine whether calcium chloride administration is a useful adjunct to blood transfusion during hemorrhagic hypotension in hypermagnesemic gravid ewes. Sixteen experiments were performed in eight chronically instrumented animals between 0.8 and 0.9 of timed gestation. The experimental sequence included (a) T = 0: magnesium sulfate 4 g IV; (b) T = 5: infusion of magnesium sulfate 4 g/h IV; (c) T = 90: maternal hemorrhage 20 mL/kg over 55 min; (d) T = 147: calcium chloride 10 mg/kg or normal saline (NS-control) 0.1 mL/kg IV; (e) T = 160: transfusion of collected maternal blood over 55 min. Magnesium sulfate alone slightly decreased maternal mean arterial pressure (P = 0.002) and increased uterine blood flow (P = 0.0001) in both groups before hemorrhage. During hemorrhage, maternal mean arterial pressure, cardiac output, and uterine blood flow, and fetal PO2 and pH all decreased sharply (P = 0.0001). Cardiac output increased (P = 0.0005) modestly just after the intravenous bolus of calcium chloride. Maternal mean arterial pressure was significantly higher (P = 0.03) during transfusion in the calcium chloride group than in the NS-control group, but only after mean arterial pressure was near baseline measurements. Maternal uterine blood flow and fetal PO2 and pH responses over time were similar in the two groups. We conclude that intravenous administration of calcium chloride (10 mg/kg) transiently increased cardiac output during hemorrhagic hypotension and slightly increased mean arterial pressure during transfusion in hypermagnesemic gravid ewes.(ABSTRACT TRUNCATED AT 250 WORDS)