Concentration of sodium, potassium, calcium and chlorides in peripheral blood and in cerebrospinal fluid in patients after strokes.
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The occurrence of respiratory alkalosis and potential benefit derived from treatment were examined in thermostressed 4-week-old broiler chicks. Blood pH was greater (P less than .05) in heat-stressed (32 C) panting birds (7.395) than either nonpanting (7.28) or birds raised at 24 C (7.28). Acute thermostress, obtained by elevating ambient temperature from 32 to 41 C over a 20-min period further elevated (P less than .05) blood pH to 7.521. Chronic heat-stressed broiler chicks suffer from intermittent respiratory alkalosis during panting; with acute heat stress, chicks pant continuously and suffer from alkalosis. Including .5% sodium bicarbonate (NaHCO3) in the diet of birds subjected to chronic heat stress enhanced body weight gain by 9% even though it tended (P less than .10) to increase blood pH in nonpanting birds. Adding .3 or 1% ammonium chloride (NH4Cl) to diets decreased blood pH (P less than .01) to 7.194 and increased (P less than .05) body weight gains by 9.5 and 25%, respectively. Effects appeared linear with NH4Cl dose to 1% NH4Cl, but 3% NH4Cl elevated weight gains by only 8% and precipitated blood acidosis (pH 7.09) in nonpanting birds. Supplementing the 1% NH4Cl diet with .5% NaHCO3 increased weight gains an additional 9%. Manipulating sodium: chloride ratios by addition of calcium chloride increased body weight gain 8% and slightly reduced severity of alkalosis. Data indicate that blood alkalosis limits growth rate of broiler chicks reared under chronic thermostress and that the respiratory alkalosis and weight gain depressions attributed to thermostress can be partially alleviated dietarily.
Exogenous citrate load from blood transfusion during orthotopic liver transplantation is thought to be the main cause of ionized hypocalcemia, which may result in hemodynamic instability. This implies that if no blood is transfused, chelation of free ionized calcium (Ca(++)) by citrate is avoided and supplemental calcium need not be given. For this study, we divided 39 pediatric living-donor liver transplant patients into two groups according to the blood component replacement given: group I received packed red blood cells and fresh frozen plasma with and without 5% albumin, and group II received 5% albumin alone. The intra-operative serial ionized calcium level was recorded, and the amount of calcium chloride replacement to maintain acceptable blood Ca(++) levels was compared between the groups. The mean serum ionized calcium level changes of both groups could be maintained within lower-to-normal limits intra-operatively. The amount of supplemental calcium chloride required to correct the hypo-ionized calcium was not significantly different between the groups. We can conclude that if an exogenous citrate load is eliminated by the avoidance of blood transfusion and 5% albumin infusion is used, instead, to replace the blood and ascites loss during OLT, the risk of ionic hypocalcemia still persists. Serum Ca(++) monitoring and adequate replacement are, therefore, still required in this setting.
The effect of calcium chloride and nifedipine on prolactin-(PRL) induced analgesia was studied by chemical assay and compared with other analgesics like morphine, thyrotrophin-releasing hormone (TRH) and clonidine. Nifedipine potentiated the analgesic effect of PRL similar to morphine while that of clonidine and TRH remained unaltered. Further, calcium chloride administration antagonized the analgesic effect of PRL and of morphine. These data suggest that PRL, similar to morphine, may alter calcium movements across the membrane to produce analgesia.
A calcium-soluble protein isolate (CSPI) was prepared from the supernatant obtained after addition of 0.75 M calcium chloride to a pH 5.0 aqueous extract of yellow mustard (Sinapis alba) seed meal. Total amino acid analysis showed that the CSPI has significantly higher (p < 0.05) contents of glutamic acid + glutamine, cysteine, and proline when compared to the precipitated, calcium-insoluble proteins. Peptide mass fingerprinting of tryptic peptides of the major polypeptides by mass spectrometry indicated that the CSPI is composed mainly of cruciferin proteins with a contribution from napins (the major allergenic proteins of S. alba). The S. alba CSPI had significantly higher (p < 0.05) protein solubility and emulsion formation ability in the presence of 0.75 M calcium chloride when compared to similar isolates prepared from Brassica juncea (brown mustard) and soybean seed meals. We suggest that the S. alba CSPI could be used to prepare calcium-fortified high protein liquid products. However, the presence of allergenic proteins in this extract may limit its widespread food use.
The effects of magnesium sulfate at different concentrations were investigated in isolated rings of uterine arteries from pregnant and nonpregnant patients. Addition of magnesium sulfate (0.5 to 9.6 mmol/L) to the suffusion medium containing the normal concentration of 1.2 mmol/L magnesium sulfate produced concentration-dependent relaxation of norepinephrine (1 mumol/L)-induced or potassium chloride (35 mmol/L)-induced contractions. Magnesium sulfate was about three times more potent in causing inhibition of potassium chloride-induced contractions in uterine arteries from pregnant patients than in those from nonpregnant patients. The concentrations that inhibited 50% of the contraction induced by potassium chloride were 0.6 +/- 0.2 mmol/L (n = 4) in the arteries from pregnant patients and 1.6 +/- 0.2 mmol/L (n = 4) in the arteries from nonpregnant patients. At high concentrations (4.8 and 9.6 mmol/L), magnesium sulfate also was more potent in inhibiting norepinephrine-induced contractions in arteries from pregnant women than in arteries from nonpregnant women. The magnesium sulfate-induced relaxation was almost completely inhibited by calcium chloride (2 mmol/L) added to the suffusion medium containing the normal concentration of 2.5 mmol/L calcium chloride but was not affected by indomethacin (5 mumol/L), methylene blue (10 mumol/L), or removal of the endothelium. The results show that magnesium sulfate, at therapeutic blood concentrations, acts as a potent dilator of human uterine arteries, especially those from pregnant patients. The results are consistent with the view that magnesium sulfate may facilitate uteroplacental perfusion.
The essential minerals calcium and zinc serve unique functions in higher organisms, and it is well recognized that homeostatic mechanisms are involved in regulating their metabolism. However, it has been reported that zinc, at higher concentrations (1 mM), inhibits intestinal absorption of sugars and amino acids. The aim of the present work was to determine whether the inhibitory effect on L-threonine absorption across the rabbit jejunum could be modified by calcium. In media with Ca2+, zinc significantly reduced L-threonine absorption. In Ca(2+)-free media, where calcium chloride was omitted and replaced isotonically with choline chloride, the amino acid transport was not modified by zinc, but when calcium chloride was replaced isotonically with magnesium chloride, the inhibition was observed. Verapamil (blocking mainly Ca2+ transport) did not modify the inhibitory effect of zinc on L-threonine transport. When A23187 (Ca(2+)-specific ionophore) was added in media with and without Ca2+, zinc produced no change in L-threonine transport. These results suggest that calcium and zinc could have an affinity with the same chemical groups of the enterocyte membrane, which would be related to the intestinal absorption of amino acids.
1. This study has defined the positive inotropic responses to the sodium channel modulator BDF 9148 in rats with hypertension, thyroid dysfunction, diabetes or dwarfism. Concentration-response curves to BDF 9148 and calcium chloride were determined in isolated left atria and left ventricular papillary muscles. 2. BDF 9148 increased force of contraction in left ventricular papillary muscles in all disease states with maximal responses comparable to calcium chloride. BDF 9148 potency was significantly decreased in muscles from diabetic rats only. 3. BDF 9148 produced similar responses in left atria except from hyperthyroid rats where negative inotropic responses only were measured. This exception confirms that the left atria is an imperfect model for ventricular responsiveness. 4. Thus, the increase in force of contraction in the ventricles as a consequence of sodium channel modulation by BDF 9148 is maintained in these disease states unlike responses to alpha-or beta-adrenoceptor agonists.
Electrophysiological study performed with the voltage clamp technique was used to examine the intracellular calcium pathway activated by tyrosine kinase receptor members. Three FGF receptors from Pleurodeles PR1, PR3, PR4, homologs to human receptors, and the human EGF receptor were expressed in Xenopus oocytes. Under FGF1, FGF2 and FGF4 stimulation, PR1 and PR3 display a one phase inward chloride calcium dependent current superimposed by sustained oscillations, whereas PR4 did not show any oscillations. These currents were dependent on intracellular calcium mobilisation, as the responses were reduced by caffeine (10 mM). Solely PR4 responses were affected by an extracellular calcium depleted solution suggesting the involvement of concomitant extracellular and intracellular calcium intervention in the calcium chloride current, whereas PR1 and PR3 did not. Under EGF stimulation, the EGF receptor elicits a two component inward current composed of an undelayed rapid transient dependent on intracellular calcium store recruitment followed by a second slower current dependent on calcium influx. The specific pattern and amplitude of the calcium oscillations induced by the combinatorial action of growth factors on their receptors could be relevant in numerous calcium dependent cell functions.
Use of a retrograde infusion system for concurrent intravenous administration of two incompatible drugs separated by a barrier fluid was studied. Four different barrier fluids (5% dextrose injection, 10% dextrose injection, 0.9% sodium chloride injection, and sterile water for injection) were used to separate sodium bicarbonate and calcium chloride. The primary infusion was 5% dextrose injection. The delivery system was visually inspected for formation of precipitate (calcium carbonate) upon addition of the two drug solutions and 2 ml of the barrier fluid. If precipitation occurred, the procedure was repeated, increasing the volume of barrier fluid incrementally until no precipitate could be seen. If no precipitate was seen with the initial 2 ml of barrier fluid, the volume of barrier fluid was decreased until precipitation occurred. These procedures were repeated for each barrier fluid at flow rates of 5-20 ml/hr for 90 minutes. The minimum volume of barrier fluid needed to prevent precipitate formation was determined in triplicate at each flow rate. The minimum volume of barrier fluid that prevented precipitate formation was approximately 2.0 ml. This volume did not differ significantly by barrier solution type or by flow rate. Sodium bicarbonate and calcium chloride can be administered concurrently by the retrograde intravenous method without visual incompatibility when separated by greater than or equal to 2 ml of barrier fluid, and this method can probably be used for administration of other potentially incompatible drugs.
A 71-years-old patient, undergoing mitral valve repair for degenerative valvulopathy and correction of pectus excavatus experienced a cardiogenic shock after weaning from cardiopulmonary bypass. The shock occurred after calcium chloride administration and was unresponsive to inotropic drugs. Transoesophageal echocardiography showed left ventricular outflow tract obstruction due to systolic anterior motion (SAM) of the mitral valve. Discontinuation of inotropic drugs and volume expansion restored the haemodynamic status. By its haemodynamic effects calcium chloride can cause left ventricular outflow tract obstruction, recognized by transoesophageal echocardiography.
In view of the USP requirement that the label of certain parenteral products contain the osmolarity of the solution, actual and theoretical osmolarity values for six preparations were determined, and the extent of any deviation was noted. Osmolarity values were determined experimentally by osmometry and converted to osmolarity values for six products: Calcium Chloride Injection USP, Dextrose Injection USP, Mannitol Injection USP, Potassium Chloride Injection USP, Sodium Bicarbonate Injection USP, and Sodium Chloride Injection USP. Theoretical values were calculated according to a standard equation based on the mass of the substance per liter of solution. The most substantial deviations between actual and theoretical osmolarity values occurred with the calcium chloride, sodium bicarbonate, potassium chloride and dextrose solutions. It is proposed that the technology for making osmotic measurements which exists in the industrial setting should be used to provide clinical practitioners with accurate and actual values. It is also urged that the USP specify a procedure for measuring osmolality and calculating actual osmolarity.
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Cytochrome c peroxidase oxidises hydrogen peroxide using cytochrome c as the electron donor. This enzyme is found in yeast and bacteria and has been also described in the trematodes Fasciola hepatica and Schistosoma mansoni. Using partially purified cytochrome c peroxidase samples from Fasciola hepatica we evaluated its role as an antioxidant enzyme via the investigation of its ability to protect against oxidative damage to deoxyribose in vitro. A system containing FeIII-EDTA plus ascorbate was used to generate reactive oxygen species superoxide radical, H2O2 as well as the hydroxyl radical. Fasciola hepatica cytochrome c peroxidase effectively protected deoxyribose against oxidative damage in the presence of its substrate cytochrome c. This protection was proportional to the amount of enzyme added and occurred only in the presence of cytochrome c. Due to the low specific activity of the final partially purified sample the effects of ascorbate and calcium chloride on cytochrome c peroxidase were investigated. The activity of the partially purified enzyme was found to increase between 10 and 37% upon reduction with ascorbate. However, incubation of the partially purified enzyme with 1 mM calcium chloride did not have any effect on enzyme activity. Our results showed that Fasciola hepatica CcP can protect deoxyribose from oxidative damage in vitro by blocking the formation of the highly toxic hydroxyl radical (.OH). We suggest that the capacity of CcP to inhibit .OH-formation, by efficiently removing H2O2 from the in vitro oxidative system, may extend the biological role of CcP in response to oxidative stress in Fasciola hepatica.
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We have developed a novel method called Calfection for gene delivery to and protein expression from suspension-cultivated mammalian cells. Plasmid DNA was simply diluted into a calcium chloride solution and then added to the cell culture for transfection. We evaluated and optimized this approach using suspension-adapted HEK293 cells grown in 12-well plates that were shaken on an orbital shaker. Highest expression levels were obtained when cells were transfected at a density of 5x10(5) cells/ml in the presence of 9 mM calcium and 5 microg/ml of plasmid DNA while maintaining a culture pH of 7.6 at the time of transfection. Suspension-adapted BHK 21 and CHO DG 44 cells could also be transfected using this method. Calfection differs from the widely known calcium phosphate coprecipitation technique. The physico-chemical composition of the DNA interacting complexes is not yet known. The transfection cocktail, DNA in a calcium chloride solution, remained highly efficient during long-term storage at temperatures ranging from room temperature to -80 degrees C. In contrast, calcium phosphate-DNA cocktails are only efficient for gene transfer when prepared fresh. Furthermore, passing the calcium-plasmid DNA mixture through a 0.2-microm filter did not compromise protein expression, whereas calcium phosphate-DNA coprecipitates were retained by the filter. High protein expression levels, a limited number of manipulations and the possibility to filter the cocktail make the Calfection approach suitable for both large-scale transfection in bioreactors and for high-throughput transfection experiments in microtiter plates.
The effects of oral calcium loading on blood pressure (BP) of DOCA (deoxycorticosterone acetate)-salt hypertensive rats (D-S rats) were investigated. Calcium loading was performed by adding 1% CaCl2 (calcium chloride) to the drinking water. Calcium loading attenuated the development of high BP in D-S rats, and at the end of a two week experiment, BP was 141 +/- 3 (calcium treated) vs. 174 +/- 7 mmHg (non-calcium treated) (p less than 0.01). However, calcium loading did not cause any changes in BP in normotensive rats. Further, in established D-S rats [after four weeks of DOCA and 1% NaCl (sodium chloride) treatment], calcium loading for 4 weeks also reduced BP [144 +/- 6 (calcium treated) vs. 181 +/- 4 mmHg (non-calcium treated), p less than 0.01, at the end of experiment]. With calcium treatment, there were no significant changes in sodium-water balance, plasma levels of epinephrine and norepinephrine, plasma renin activity, plasma aldosterone concentration and serum electrolytes both in developing and established D-S rats. The depressor mechanism of calcium loading was studied by observing vascular responsiveness to norepinephrine both in whole body and in hind limb preparations. Vascular reactivity in both developing and established D-S rats was significantly attenuated by calcium treatment. These results suggest that the antihypertensive effects of calcium treatment in D-S rats are mainly caused by attenuation of vascular reactivity.
In order to evaluate the effects of the combination of halothane and verapamil on left ventricular function and coronary blood flow (CBF), six sheep were anaesthetized with halothane (1.2% inspired) and given increasing cumulative doses of intravenous verapamil. Regional myocardial function was assessed by sonomicrometry in the areas supplied by the left anterior descending coronary artery (LAD) and the left circumflex coronary artery (LC). Changes in global haemodynamics, atrioventricular conduction, LV relaxation and systolic shortening after 0.32 mg X kg-1 intravenous verapamil indicated impaired left ventricular function. Significant myocardial dysfunction (post-systolic shortening) occurred in the LAD territory, accompanied by a 64% decrease (42 +/- 6 to 15 +/- 3, P less than 0.01) in coronary perfusion pressure (CPP). Coronary blood flow in the LC segment decreased 83% (102 +/- 15 to 17 +/- 13, P less than 0.01) as coronary reserve was exhausted with the decrease in CPP. Calcium chloride reversed the impairment of global and regional myocardial function observed with verapamil, improved the impaired left ventricular relaxation, but did not significantly alter atrioventricular conduction. Thus the combination halothane-verapamil can cause significant left ventricular depression and myocardial dysfunction, possibly by inducing subendocardial ischaemia or by direct pharmacologic effect. Calcium chloride reverses this regional myocardial dysfunction as well as the deleterious global haemodynamic changes caused by halothane-verapamil; however, the changes in atrioventricular conduction are not corrected by calcium.