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PubMed1980

Stimulation by calcium chloride of virus-induced interferon formation by blood, haemopoietic organ and continuous human cells.

Calcium chloride stimulated virus-induced production of leukocyte interferon by human and animal blood and haemopoietic organ cells. CaCl2 treatment of surviving cells (leukocytes, human and mouse bone marrow) and Namalva cells was the most effective when carried out simultaneously with adsorption of the virus-inducer or when CaCl2 pretreatment was combines with its subsequent addition together with the virus-inducer. Optimal CaCl2 concentrations were 5 mM for human bone marrow cells and 10 mM for human leukocytes and mouse bone marrow cells. CaCl2 treatment was equivalent to priming in case of interferon induction in human leukocytes and, as distinct from priming, it considerably increased virus-induced interferon production by Namalva cells.

Animals↗
PubMed1997

Tenderizing spent fowl meat with calcium chloride. 3. Biochemical characteristics of tenderized breast meat.

Biochemical characteristics of spent fowl meat injected with calcium chloride or sodium chloride were evaluated. Hot-boned breast fillets were injected to 10% (wt/wt) with 0.3 M CaCl2 or 0.6 M NaCl, tumbled, and aged 24 h. Tumbling was conducted at 20 C, -635 mm Hg, 20 rpm for 1 h. Hot-boned and cold-boned (24 h) fillets were used as controls. One fillet from each carcass was baked and sheared with an Allo-Kramer cell, whereas the other fillet was used for biochemical analysis. Shear values indicated that both CaCl2- and NaCl-treated samples had significantly (P < 0.05) lower shear values than hot-boned controls but were similar (P > 0.05) to cold-boned samples. The CaCl2 injection treatment significantly elevated (P < 0.05) the tissue calcium content compared to all other treatments. There was no significant difference in heat-stable collagen content (P > 0.05) among all treatments, which indicated that CaCl2 or NaCl did not contribute to meat tenderness through degradative changes in collagen. Calpain data indicated that mu-calpain had disappeared by 24 h aging in all treatments. The m-calpain activity was significantly lower (P < 0.05) in samples treated with CaCl2 than in the other samples. The NaCl-treated samples had m-calpain activity similar (P > 0.05) to that of hot-boned controls. Sarcomeres of CaCl2-treated samples were significantly shorter (P < 0.05) than those of cold-boned controls, were similar (P > 0.05) to those of hot-boned controls, and were shorter than those of NaCl-treated muscles. The sarcomere length and calpain data suggest that CaCl2 tenderized fillets by ionic strength and calcium-specific effects (possibly a proteolytic action), whereas the NaCl solution tenderized by ionic strength effect at a similar conductivity level to that of the CaCl2 solution.

Animals↗
PubMed1983

Haemodynamic effects of calcium chloride administered intravenously to patients with and without cardiac disease during neurolept anaesthesia.

During neurolept anaesthesia, calcium chloride (15 mg/kg) was administered intravenously to two different groups of patients undergoing vascular surgery on the abdominal aorta. The patients in group I all suffered from cardiac disease and were treated with digoxin, while the patients in group II had no cardiac symptoms. Cardiovascular measurements were made during steady-state anaesthesia. In group I, CaCl2 increased cardiac index (CI) significantly while systemic vascular resistance index (SVRI) remained unchanged. Mean arterial pressure (MAP) increased. In group II, both MAP and SVRI increased while CI remained unchanged. No significant changes in heart rate were observed and no arrhythmias occurred. It is concluded that CaCl2 administered intravenously is an effective means of improving cardiac function when it is depressed by anaesthesia, underlying cardiac disease, or both.

Aged↗
PubMed1984

Hemodynamic effects of calcium chloride in adults with regurgitant valve lesions.

We evaluated the hemodynamic effects of 7 mg/kg intravenous calcium chloride (CaCl2) or placebo in 20 adults with regurgitant aortic and/or mitral valves before and after induction of anesthesia with fentanyl (50 micrograms/kg), followed by pancuronium (0.1 mg/kg) and 100% oxygen. CaCl2 produced no changes in mean systemic, pulmonary arterial, central venous, or pulmonary capillary wedge pressures or vascular resistances before or after induction of anesthesia. A significant increase in left ventricular stroke work index was seen 1 min after CaCl2 was administered after induction of anesthesia (from 31.29 +/- 3.00 to 37.44 +/- 3.81 g X m X M-2). Before induction, CaCl2 decreased heart rate from 93.9 +/- 9.6 to 85.2 +/- 8.7 beats/min (statistically significant 2.5 and 10 min after CaCl2) and after induction from 104.6 +/- 8.4 to 89.3 +/- 7.5 (significant at 1, 2.5, 5, and 10 min). These results suggest that CaCl2 is associated with an immediate increase in ventricular performance and that the subsequent decrease in heart rate is not sufficient to contraindicate use of CaCl2 as an inotrope in patients with chronic valvular regurgitation. The effects of CaCl2 injection in man on pulmonary shunt fraction (Qs/Qt) have not been described previously. We found no change in Qs/Qt, suggesting that CaCl2 has no direct effect on distribution of pulmonary blood flow.

Aortic Valve Insufficiency↗
PubMed2000

Effects of calcium chloride on grafted internal mammary artery flow after cardiopulmonary bypass.

OBJECTIVE: To examine the effects of calcium chloride (CaCl2) administration on blood flow through the grafted left internal mammary artery (IMA) after cardiopulmonary bypass (CPB). DESIGN: Single-arm prospective study. SETTING: University-affiliated hospital operating room. PARTICIPANTS: Twenty adult patients scheduled for coronary artery bypass graft surgery with IMA graft. INTERVENTIONS: IMA flow was measured noninvasively with a laser Doppler flow probe placed around the IMA, and measurements were recorded for 10 seconds and averaged. After separation from CPB under stable hemodynamics, baseline IMA flow was measured. CaCl2, 15 mg/kg, was administered intravenously over 1 minute. Blood pressure, left atrial pressure, heart rate, and IMA flow were then measured at 1, 5, and 10 minutes. Coronary perfusion pressure and IMA vascular resistance were calculated. MEASUREMENTS AND MAIN RESULTS: After CaCl2 administration, IMA blood flow significantly decreased from baseline at 1, 5, and 10 minutes (from 28+/-9 mL/min to 19+/-8 mL/min, 22+/-6 mL/min, and 25+/-4 mL/min), with gradual return toward baseline over time. Blood pressure, coronary perfusion pressure, and IMA vascular resistance significantly increased at 1 and 5 minutes after CaCl2. Left atrial pressure and heart rate remained unchanged. No systolic regional wall motion abnormalities were detected on transesophageal echocardiography. CONCLUSIONS: CaCl2, administered as a bolus dose after separation from CPB, transiently but significantly reduces IMA flow and can potentially trigger vasospasm, increasing the risk for myocardial ischemia or infarction in susceptible patients. Further studies are needed to determine whether this effect also occurs with nitrosodilators or phosphodiesterase inhibitors.

Aged↗
PubMed1985

Influence of heparin and calcium chloride on assay, stability, and recovery of factor VIII.

The influence of heparin alone or in conjunction with calcium chloride on the coagulation assay for factor VIII, on the stability of factor VIII in blood and in plasma, and on the recovery of factor VIII in cryoprecipitate and in an intermediate purity concentrate was investigated. A stabilizing effect of heparin and calcium on factor VIII activity in blood and plasma could be confirmed. We were, however, unable to make use of the higher activity that can, under certain circumstances, be recovered in the cryoprecipitates; this was mainly due to the poor solubility of cryoprecipitates prepared from heparinized blood. Heparin (or the absence of a calcium chelator) also interferes with the recovery of plasma components other than factor VIII.

Calcium Chloride↗
PubMed1996

Hemodynamic effects of calcium chloride in a canine model of acute propranolol intoxication.

STUDY OBJECTIVE: To evaluate the hemodynamic effects of calcium chloride in a canine model of acute propranolol toxicity. METHODS: Two minutes after the completion of a propranolol infusion (10 mg/kg), a bolus of .125 mL/kg 10% CaCl solution followed by an infusion of .375 mL/kg over the next 30 minutes or a bolus and subsequent infusion of an equivalent volume of normal saline solution was administered to each dog. RESULTS: CaCl yielded significant improvements in propranolol-induced decreases in cardiac index and stroke volume compared with saline solution-treated control animals (overall alpha = .05). Furthermore, CaCl administration resulted in earlier improvement in propranolol-induced alterations in mean arterial pressure, maximal left ventricular pressure change over time, and peripheral vascular resistance compared with saline solution (overall alpha = .05). We observed no difference between treatment groups in response to propranolol-induced bradycardia or QRS-interval prolongation. CONCLUSION: In this model of acute propranolol toxicity, CaCl therapy improved depressed hemodynamic status, mainly by a positive inotropic action.

Acute Disease↗
PubMedDate not supplied

[Comparative characteristics of the activity of lithium preparations and anti-arrhythmia agents in strophanthin, calcium chloride and barium chloride arrhythmias in an experiment].

During disorders of cardiac rhythm induced by strophanthine K in anesthesized cats, by calcium chloride in mice and anesthesized rats, and by barium chloride in rabbits, lithium hydroxybutyrate (0.55-3.2 mg/kg according to cation) compares very favourably with lithium chloride, novocainamide, lidocaine, trimecaine, etmozine, quinidine and verapamil as regards antiarrhythmic activity and the range of therapeutic action.

Animals↗
PubMedDate not supplied

Formation of alginate microspheres produced using emulsification technique.

This study investigated the formative process of alginate microspheres produced using an emulsification technique. The alginate microspheres were produced by cross-linking alginate globules dispersed in a continuous organic phase using various calcium salts: calcium chloride, calcium acetate, calcium lactate and calcium gluconate. The size, shape, drug content and Ca2+ content of the microspheres were evaluated. The tack, viscosity and pH of the calcium salt solution and percentage of Ca2+ partitioned into the organic phase were determined. Microscopic examination of the test emulsion at various stages of the emulsification process was also carried out. The propensity of cross-linking reaction was found to be dependent on successful collision between alginate and calcium salt globules. Examination of the characteristics of microspheres indicated that the formed microsphere was a resultant product of alginate globule clustering. The growth propensity of microspheres was promoted by the higher rate and extent of cross-linkage which was governed by the pH, tack and/or Ca2+ content of the cross-linking solution, as well as the dissociation constant and diffusivity of the calcium salt. Overall, the amount of free Ca2+ cross-linked with alginate in the formed microspheres was in the following order: calcium acetate > calcium chloride + calcium acetate > calcium chloride + calcium gluconate; calcium chloride + calcium lactate > calcium chloride. In microencapsulation by emulsification, the mean size of the microspheres produced can be modified by varying the tack, pH and Ca2+ content of the cross-linking solution and through the use of a combination of calcium salts. The shape of the microspheres produced was, nonetheless, unaffected by the physicochemical properties of the cross-linking solution.

Alginates↗
PubMed1978

[Effect of intravenous administration of calcium chloride on the effectiveness of infusion therapy of acute massive blood loss].

In acute experiments on 70 dogs at the late stage of the organism response to acute massive blood loss hemotransfusions, infusion of decalcinated gelatinol, or of a 0.9% solution of sodium chloride were incapable of preventing death of the animals. Intravenous infusions of a 10% calcium chloride solution following such therapy promoted survival of most of the animals.

Animals↗
PubMedDate not supplied

[Reference values of sodium, potassium, chloride, calcium, inorganic phosphate and magnesium levels in the cerebrospinal fluid of children].

Concentration of sodium, potassium, chloride, calcium, inorganic phosphate and magnesium was determined in cerebrospinal fluid of 155 children (ages 1 month - 16 years). On the basis of clinical criterions the children were considered to be "healthy". The total number of examined children was 2 500 (1978-1983). The statistical age- and sexspecific investigation of the results showed no significant differences. Compilation of the values resulted in a physiological concentration of sodium 132.3 +/- 17.6 mval/l, potassium 2,59 +/- 0.37 mval/l, chloride 113.1 +/- 15.5 mval/l, calcium 3.47 +/- 1.45 mval/l, inorganic phosphate 1.11 +/- 0.21 mg/dl and magnesium 2.60 +/- 0.46 mg/dl.

Adolescent↗
PubMed1988

Aneurysm of the rabbit common carotid artery induced by periarterial application of calcium chloride in vivo.

Experimental aneurysmatic dilatation of the rabbit common carotid artery was induced by a single, periarterial application of calcium chloride in vivo. Vessels were fixed in situ after 3 d, 1 wk, 3 wk, 6 wk, and 12 wk by intracardiac perfusion of glutaraldehyde and tissues prepared for light, scanning, and transmission electron microscopy. Progressive focal aneurysmal dilatation was seen limited to the site of calcium application with endothelial damage and thrombus formation in areas of irregular luminal contour. Disruption of the elastic network of the intima and media was seen with varying degrees of intimal fibromuscular hyperplasia and medial disorganization. The calcium-elastic tissue complex was the focus of the inflammatory, arteriosclerotic reaction and subsequent aneurysm formation. The inflammatory cell infiltration initially included primarily neutrophils followed by lymphocytes, plasma cells, monocytes, and multinucleated giant cells. These studies support the hypothesis that disruption of the elastic tissue network of the vascular wall represents an important pathogenetic factor in the initiation of aneurysmal dilatation. In addition, the results of these studies suggest that interaction of calcium with the elastica of the arterial wall may represent an important pathogenetic factor in the initiation of giant cell arteritis.

Aneurysm↗
PubMed1984

Hemodynamic effects of calcium chloride injection following cardiopulmonary bypass: response to bolus injection and continuous infusion.

To determine the hemodynamic effects of intravenous injection of calcium chloride, 26 patients were studied immediately after termination of extracorporeal circulation. Eighteen patients (Group A) had injection of a single bolus of CaCl2; in the other 8 patients (Group B), the bolus injection was followed by infusion of CaCl2 at a rate of 1.5 mg/kg/min for 10 minutes. Myocardial contractile element velocity (Vpm), aortic blood flow, electrocardiograms, and left ventricular, systemic arterial, pulmonary arterial, and left atrial pressures were recorded continuously. The baseline ionized calcium level after bypass was 3.6 +/- 0.6 mg/100 ml (normal range, 3.9 to 4.5 mg/100 ml); this increased to 5.4 +/- 0.5 mg/100 ml 1 minute after CaCl2 injection. The ionized calcium level was 4.7 +/- 0.6 mg/100 ml 6 minutes after CaCl2 injection in Group A, and was 5.9 +/- 0.2 mg/100 ml and 6.4 +/- 0.2 mg/100 ml at 6 and 10 minutes, respectively, in Group B. There was significant early hemodynamic improvement after CaCl2 injection, including increases in Vpm (p less than 0.001), cardiac index (p less than 0.001), mean blood pressure (p less than 0.01), and stroke volume index (p less than 0.001). A similar pattern of hemodynamic response was observed in both groups. Approximately 1 minute after CaCl2 injection, cardiac index returned to control level, Vpm and mean blood pressure remained elevated, and heart rate declined (p less than 0.01). Systemic vascular resistance gradually increased and was significantly elevated (p less than 0.05) in Group B at 3 minutes and in Group A at 6 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1978

[A short loading acidificacion test with calcium chloride in infants (author's transl)].

The response of blood and kidney to orally administered CaCl2 (4.1 mEq. X Kg.) in a short acid loading was compared to that attained with standard agent NH4Cl (3.9 mEq. X Kg) in two groups of normal infants through a 6 hrs. period. Plasma pH and bicarbonate decreased significantly. Minimum urine pH was 5.0 o lesser in all infants. Decrease of urine pH was greater to CaCl2 than to NH4Cl group but the net hydrogen ion excretion by the kidney was minor. Accordingly this experience CaCl2 can replace NH4Cl as acidifying substance in a short acid loading test. Indication will be diffuse hepatic lesions rendering dangerous NH4Cl administration.

Acidosis, Renal Tubular↗