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PubMed2006

Preparation and in vitro evaluation of mucoadhesive properties of alginate/chitosan microparticles containing prednisolone.

This study describes the preparation of mucoadhesive alginate/chitosan microparticles containing prednisolone intended for colon-specific delivery. Two methods have been used for the preparation of the particles: the one-step method is the method in which prednisolone was dispersed within sodium alginate solution and this dispersion was then dropped in a solution containing both calcium chloride and chitosan. The two-step method consisted also of the dispersion of prednisolone in alginate solution and then dropping this dispersion into a solution containing calcium chloride, the particles were then transferred to a chitosan solution. The concentration of sodium alginate solution at 2% (w/v), various concentrations of calcium chloride solution (0.5-1.0%, w/v), chitosan solutions (0.5, 1.0 and 1.5%, w/v) and prednisolone drug load (2, 5, 10 and 15%, w/v) have been used. The results for both preparation methods show that the particle size and drug content were mainly depending on the amount of the drug concentration and not the amount of chitosan and calcium chloride. The in vitro mucoadhesive tests for particles prepared from both methods were carried out using the freshly excised gut of pigs. The particles prepared by the one-step method exhibited excellent mucoadhesive properties after 1h test. Increased chitosan concentrations from 0, 0.5, 1.0 to 1.5% (w/v) resulted in 43, 55, 82 and 88% of the particle remaining attached on the gut surface after 1 h, respectively. However, the particles prepared by the two-step method showed significant less mucoadhesion under the same experimental conditions. At chitosan concentrations of 0, 0.5, 1.0 and 1.5% (w/v) the amount of particles remaining attached to the mucosal surface of the pig gut after 1 h was 43, 3, 11 and 11%, respectively. The prednisolone release at a pH of 6.8 after 4 h was between 63 and 79% for the particles prepared by the one-step method and between 57 and 88% for the particles prepared by the two-step method with a prednisolone drug load of 5 and 10% (w/v), respectively. The results show that depending on the preparation method these chitosan coated alginate particles show different mucoadhesiveness whereas their other properties are not statistically significant different.

Adhesiveness↗
PubMed1992

Cardiac responses after norepinephrine-induced ventricular hypertrophy in rats.

The increase in norepinephrine (NE) blood levels in human heart failure correlates with prognosis. In this study, we determined whether continuous NE infusion alters the positive inotropic and chronotropic responses of isolated rat cardiac muscles. Osmotic minipumps were implanted subcutaneously (s.c.) in 43 adult male rats to deliver NE (160 micrograms/kg/h for 14 days); 42 rats were sham-operated. Isolated left and right atria and left and right ventricular (LV, RV) papillary muscles were prepared to measure positive inotropic or chronotropic responses to NE, phenylephrine, forskolin, dibutyryl cyclicAMP (dbcyclicAMP), and calcium chloride. NE infusion caused (a) a 22% increase in LV wet weight without altering atrial or RV wet weights; (b) an 18% decrease in maximal inotropic response to calcium chloride in LV papillary muscles only; (c) a significantly decreased peak response to NE [72 +/- 5 vs. 93 +/- 5% (sham rats) of calcium chloride] but not to forskolin or dbcyclicAMP in RV papillary muscles; (d) an increased incidence of ectopy at low concentrations of NE, forskolin, and dbcyclicAMP in LV papillary muscles; (e) no alteration in papillary muscle responses to phenylephrine but significantly increased left atrial inotropic responses [51 +/- 5 vs. 33 +/- 2% (sham rats) of calcium chloride] and right atrial chronotropic responses [30 +/- 2 vs. 18 +/- 4 (sham rats) beats/min]; and (f) a selective decrease in beta 1-adrenoceptor density in both ventricles. Thus, NE infusion causes selective LV hypertrophy; responses of compounds that increase intracellular cyclicAMP are affected to a greater extent in papillary muscles from the hypertrophied ventricle than in tissues from the other chambers of the heart.

Animals↗
PubMed1992

Interaction between stannous chloride and calcium channel blockers in frog neuromuscular transmission.

We have investigated the interactions between stannous chloride (SnCl2) and calcium (Ca) channel blockers on endplate potentials (e.p.p.) and on miniature endplate potentials (m.e.p.p.) to determine which type of channel (among L-, N-, and T-type) participates in the SnCl2-induced increase in Ca entry into motor nerve terminals. The e.p.p. amplitude augmented by 30 microM SnCl2 was decreased by cumulative addition of 10 microM CdCl2 or 0.5 microM omega-conotoxin but not by 10 microM NiCl2 or 5 microM nicardipine. The SnCl2 (30 microM)-induced rise in m.e.p.p. frequency in high-potassium medium was reduced by 0.5 microM omega-conotoxin but not by 5 microM nicardipine. These results suggest that activation of the N-type Ca channel is involved in the SnCl2-induced increase in Ca entry into the nerve terminals.

Animals↗
PubMed1998

Characterization of calcium-activated chloride channels in patches excised from the dendritic knob of mammalian olfactory receptor neurons.

We investigated the properties of calcium-activated chloride channels in inside-out membrane patches from the dendritic knobs of acutely dissociated rat olfactory receptor neurons. Patches typically contained large calcium-activated currents, with total conductances in the range 30-75 nS. The dose response curve for calcium exhibited an EC50 of about 26 microM. In symmetrical NaCl solutions, the current-voltage relationship reversed at 0 mV and was linear between -80 and +70 mV. When the intracellular NaCl concentration was progressively reduced from 150 to 25 mM, the reversal potential changed in a manner consistent with a chloride-selective conductance. Indeed, modeling these data with the Goldman-Hodgkin-Katz equation revealed a PNa/PCl of 0.034. The halide permeability sequence was PCl > PF > PI > PBr indicating that permeation through the channel was dominated by ion binding sites with a high field strength. The channels were also permeable to the large organic anions, SCN-, acetate-, and gluconate-, with the permeability sequence PCl > PSON > Pacetate > Pgluconate. Significant permeation to gluconate ions suggested that the channel pore had a minimum diameter of at least 5.8 A.

Animals↗
PubMed1991

Hemodynamic instability after the initiation of extracorporeal membrane oxygenation: role of ionized calcium.

OBJECTIVES: To prospectively document the occurrence of ionized hypocalcemia in infants and children treated with extracorporeal membrane oxygenation (ECMO), to determine if the type of calcium salt (calcium chloride or gluconate) used in priming the ECMO circuit affected ionized calcium, to determine if ionized calcium concentrations correlate with total calcium, protein, albumin, or total magnesium values, and to determine if the hypotension usually observed after ECMO initiation correlates with low circulating ionized calcium concentrations. DESIGN: Prospective study. SETTING: Pediatric ICU and neonatal ICU. PATIENTS: Sixteen neonatal and three pediatric patients who were started on ECMO for cardiopulmonary support. INTERVENTIONS: The ECMO circuit was primed in a standardized manner, 100 mg of calcium gluconate was added in group 1 patients and 100 mg of calcium chloride was added in group 2 patients. MEASUREMENTS: Ionized calcium was measured from the circuit before initiation of ECMO and from the patient before, and then 5, 10, 15, 30, 60, 120, and 240 mins after initiation of ECMO. Total calcium and ionized calcium concentrations were measured simultaneously every 6 hrs. Serum total protein, albumin, magnesium, and ionized calcium values were measured from blood samples collected simultaneously twice daily. RESULTS: A significant decrease in the mean serum ionized calcium value occurred 5 mins after the initiation of ECMO in both groups, p less than .001. The ionized calcium value remained significantly decreased until 30 mins after the initiation of ECMO. There were no differences between the ionized calcium concentrations obtained during priming with calcium gluconate vs. those concentrations obtained with calcium chloride priming (p = .79). Throughout the course of ECMO, the serum ionized calcium concentrations ranged from 0.60 to 1.86 mmol/L. Poor correlations existed between circulating ionized calcium values and total calcium (r2 = .30), total protein (r2 = .20), albumin (r2 = .20), and magnesium concentrations (r2 = .10). There was a good correlation between the patients' BP and ionized calcium concentrations after bypass was initiated (r2 = .87). CONCLUSION: Our data demonstrate that ionized hypocalcemia is a frequent occurrence after the initiation of ECMO. Since there is a poor correlation between ionized calcium and total calcium, ionized calcium concentrations should be measured directly in these patients.

Blood Pressure↗
PubMed1986

Calcium enhances the hemolytic action of bile salts.

The lysis of human erythrocytes by bile salts in buffer containing isotonic saline was dramatically enhanced by the addition of 5-10 mM calcium chloride. All bile acids tested showed this effect, with a marked increase in lysis occurring at 0.75 mM for deoxycholate, 1 mM for chenodeoxycholate, 2.5 mM for ursodeoxycholate and 5.5 mM with cholate in the presence of 10 mM calcium chloride. The effect appeared to be specific for calcium; strontium chloride and magnesium chloride gave no stimulatory effect. The increased lysis of the erythrocytes in the presence of 1 mM deoxycholate and 1-10 mM calcium chloride was not associated with increased uptake of the bile salt by the cells (measured with [14C]deoxycholate). Using erythrocytes previously labelled with [3H]cholesterol, there was no evidence of an enhanced removal of that membrane component in the presence of calcium and deoxycholate, compared to deoxycholate alone. The sensitivity of the cells to the effect of calcium in the presence of 1 mM deoxycholate increased with the length of time of their storage at 4 degrees C. The sensitivity returned to that of fresh cells after incubation at 37 degrees C with 30 mM adenosine plus 25 mM glucose, but this treatment did not further diminish the lysis. Lysis in the presence of 10 mM calcium chloride and 1 mM deoxycholate was partially blocked by increasing the KCl concentration at the expense of NaCl. The maximum effect occurred with a buffer comprising 100 mM KCl/50 mM NaCl. A more dramatic reduction in the lysis followed the incorporation of the calcium chelator, quin2, into the cells. The lysis induced by 1 mM deoxycholate in the presence of calcium was reduced by 80% in quin-2-loaded cells compared to controls. The data suggest that bile acids can promote the influx of calcium into erythrocytes, leading to lysis as a result of the efflux of intracellular potassium and/or the uptake of sodium from the incubation medium. The data further suggest that cellular effects may occur at lower bile acid concentrations than that thought to be required for detergent damage.

Aminoquinolines↗
PubMed1992

Role of elastase as a virulence factor in experimental Pseudomonas aeruginosa infection in mice.

The role of elastase and alkaline protease in the pathogenesis of fatal infections caused by Pseudomonas aeruginosa was determined in mice treated with calcium chloride. Mortality increased significantly when solutions containing elastase were injected together with non-lethal inocula of strain PA 103, which does not produce proteolytic enzyme. In contrast, solutions containing alkaline protease did not increase mortality. In mice injected intramuscularly with strain PA 103 and calcium chloride, the organisms grew rapidly in the injected muscle but not in the liver. However, when elastase was injected together with strain PA 103 and calcium chloride, viable bacteria were also found in the liver. Moreover, the survival rate of mice challenged with elastase-producing strain 5 and calcium chloride was enhanced, and colonization of the liver prevented, by immunization with elastase toxoid. These results suggest that elastase contributes to the invasiveness of the organism.

Animals↗
PubMed1988

Interaction of aminoglycoside antibiotics and calcium channel blockers at the neuromuscular junctions.

Aminoglycoside antibiotics (mmol.l-1) gentamicin (0.74), streptomycin (1.02), netilmicin (1.24), amikacin (2.23), sisomicin (2.74), dactimicin (2.75), kanamycin (3.43), kanendomycin (3.45), tobramycin (3.53) and dibekacin (4.35) produce a complete neuromuscular blockade at the isolated phrenic nerve-hemidiaphragm preparation of the rat, which is only reversed by calcium chloride. On the other hand, verapamil (2.04 mmol.l-1), a calcium channel blocker, also produces a complete neuromuscular blockade at the above preparation which is reversed by calcium chloride. Aminoglycoside antibiotics are potentially capable of interacting with verapamil and produce a complete neuromuscular blockade at concentrations significantly reduced. The neuromuscular blockade which is produced by the concurrent administration of the aminoglycoside antibiotics and verapamil is obtained with the usual therapeutic blood concentrations of the individual agents. Furthermore, the neuromuscular blockade which is produced during verapamil-aminoglycoside antibiotics interactions is completely reversed after calcium chloride administration. The mechanism by which aminoglycoside antibiotics and verapamil produce neuromuscular blockade must be the same. Both classes of drugs interfere with calcium ions movements through the calcium channels of the membrane of the motor nerve-endings inhibiting acetylcholine release at the synaptic cleft. The interaction of aminoglycoside antibiotics and calcium channel blockers is of clinical significance because when these agents are given concurrently during the perioperative period they may lead to respiratory depression or prolonged apnoea. These respiratory disturbances can be managed by slow intravenous infusion of 50 to 200 mg of calcium gluconate.

Aminoglycosides↗
PubMed1977

Effects of halothane, thiopental, and lidocaine on fluidity of synaptic plasma membranes and artificial phospholipid membranes.

The effects of halothane, thiopental, and lidocaine were studied with spin-labeling methods in synaptic plasma membranes (order parameter) and artificial phospholipid membranes (lateral diffusion). Halothane had a biphasic action, low concentrations (0.64 mM) ordering and high concentrations (2.9 mM) fluidizing both types of membranes. A biphasic effect in phospholipid membranes was also seen with thiopental, 0.1 mM ordering and 10 mM fluidizing, whereas in synaptic plasma membranes both low and high concentrations caused an increased order in the lipid bilayer region. At high thiopental concentrations, a considerable number of molecules may have reacted with membrane proteins or accumulated in the highly fluidic hydrophobic interior region of the membrane without affecting the rotational movement of the labeled fatty acid. Lidocaine alone, or together with calcium chloride, at various concentrations to 10 mM had no significant effect, and a fluidizing effect of 1 mM calcium chloride was possibly a result of interaction of calcium chloride with the label. The results indicate that the three lipid-soluble anesthetics interact differently with the lipid part of membranes. Lidocaine did not seem to affect bilyer lipids, while thiopental and halothane in phospholipid vesicles and halothane alone in synaptic membranes caused a dose-dependent biphasic effect.

Anesthesia, Inhalation↗
PubMedDate not supplied

Cyclic AMP- and calcium-activated chloride currents in Leydig cells isolated from mature rat testis.

Using the whole-cell recording technique, we have investigated some properties of the membrane currents induced by depolarization of Leydig cells isolated from mature rat testis. Internal perfusions with cyclic AMP or calcium induce currents which reveal the properties of the cyclic AMP-activated and calcium-activated chloride conductances. Both currents are sensitive to EC1 displacement and are similarly affected by SITS and DIDS, two stilbene-derived chloride channel blockers. However, at the resting membrane potential, the cyclic AMP-dependent, not the calcium dependent conductance, is activated. We discuss the involvement of these results in the physiology of the Leydig cells.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1992

Antisense oligodeoxynucleotides to the cystic fibrosis transmembrane conductance regulator inhibit cAMP-activated but not calcium-activated chloride currents.

Phosphorylation of the cystic fibrosis transmembrane conductance regulator (CFTR) by cAMP-dependent protein kinase leads to chloride flux in epithelial cells. Is CFTR also required for the calcium-dependent activation of chloride channels? We used antisense oligodeoxynucleotides to CFTR to reduce the expression of CFTR in colonic and tracheal epithelial cells. The antisense oligomers were a pair of adjacent 18-mers complementary to nucleotides 1-18 and 19-36 of CFTR mRNA. Sense and misantisense oligomers served as controls. A 48-h antisense treatment reduced the expression of CFTR protein as assayed by immunoprecipitation and autoradiography to 26% of the level in sense-treated T84 cells. Whole-cell patch clamp revealed that a 48-h antisense treatment of T84 and 56FHTE-8o- fetal tracheal epithelial cells reduced the cAMP-activated chloride current to approximately 10% of that in sense-treated cells. The half-life of functional CFTR is less than 24 h in these cells. In contrast, the calcium-activated chloride current was not affected by antisense treatment. Hence, the cAMP and calcium pathways are separate. CFTR is required for the cAMP pathway but not for the calcium pathway.

Base Sequence↗
PubMedDate not supplied

[Effect of calcium ions on adrenal glucocorticoid function].

In the experimental dogs and healthy humans it was shown that calcium ions promote activation of the adrenal glucocorticoids function, which duration is dependent on the day time. In patients the influence of calcium ions on the blood 11-hydroxycorticosteroid concentration is dependent on the initial steroid level and concentration of injected calcium chloride solution. The infusion of 1% calcium chloride solution exerted a stable effect. Possible mechanisms of the changes observed are discussed.

11-Hydroxycorticosteroids↗
PubMed1981

Parathyroid hormone, cAMP, electrolytes and uric acid after high dose CaCl2 in patients with idiopathic stone formation.

High dose levels of calcium chloride significantly decrease serum level of parathyroid hormone (PTH) in both patients with history of idiopathic stone formation and healthy controls. Suppressibility of parathyroid glands is obtained by injection of 10 ml 10% calcium chloride without any restriction in calcium diet. Serum levels of calcium measured 14 mg/dl 10 min. after high dose calcium chloride injection and distinctly affect cAMP in urine in patients when compared to healthy controls. The elimination of electrolytes and uric acid is elevated 40 min. after calcium application in both patients and controls and returns to normal values 120 min. later. No stone formation has been observed in an eighteen mouth follow up of all subjects studied.

Adult↗
PubMed1989

Calcium-activated chloride current in rat vascular smooth muscle cells in short-term primary culture.

Isolated cells from rat portal vein smooth muscle in short-term primary culture were studied using patch-clamp technique (whole-cell configuration). In order to study a calcium-activated chloride current, the potassium currents were blocked by intracellular cesium diffusion. Without EGTA in the pipette solution, depolarizing voltage pulses from a holding potential of -70 mV to positive potentials activated an early inward and a late outward current. The latter persisted as a long-lasting inward tail current when the membrane was repolarized to -70 mV. The outward current measured at the end of the pulse and the tail current were blocked by extracellular cobalt, after replacement of external calcium with barium, after removal of external calcium, and when the calcium concentration of the pipette solution was less than 0.5 microM, suggesting that they were calcium-dependent. The tail current decay was voltage sensitive, becoming faster with hyperpolarization. The reversal potential of the calcium-activated current was near the equilibrium potential for chloride ions, and was shifted as predicted by the Nernst equation when the extracellular or intracellular chloride concentration was changed. The calcium-activated current was blocked by adding micromolar concentrations of niflumic acid or millimolar concentrations of DIDS. This effect of compounds known to interfere with chloride channels together with the data on the equilibrium potential for chloride ions indicated above suggested the existence of a calcium-activated chloride current in vascular smooth muscle cells.

Animals↗
PubMed1998

Chronopharmacokinetics and calcium in the prevention of gentamicin-induced nephrotoxicity in rabbits.

The study used 36 New Zealand white rabbits organized into three groups of 12 animals each. Group I received gentamicin; Group II received joint administration of gentamicin and calcium chloride and Group III received gentamicin, calcium chloride and verapamil. All the drugs were administered over 16 day periods. Groups I and II were divided in two subgroups, one subgroup receiving the treatment in winter and the other in summer. The results obtained for Group I indicate that there is an influence of the seasonal period on the gentamicin elimination and/or distribution. Mean plasma levels of the antibiotic at steady-state as well as the amounts of gentamicin accumulated in renal tissue are higher in winter than in summer. On the other hand, when calcium was administrated with the antibiotic, no significant circannual variations were observed in the renal toxicity of gentamicin. Under our study conditions the presence of calcium diminishes gentamicin plasma levels and the amount accumulated in kidney. Calcium, probably, generated a diminution in renal damage and consequently gentamicin renal excretion increases. The differences between Group II and Group III are due to the effect of verapamil. This agent blocks the calcium channels reducing the calcium protective effect on the nephrotoxicity of gentamicin.

Animals↗
PubMed2001

Insulin and IGF-I inhibit calcium-dependent chloride secretion by T84 human colonic epithelial cells.

D-Myo-inositol (3,4,5,6) tetrakisphosphate [Ins(3,4,5,6)P(4)] or phosphatidylinositol 3-kinase (PI 3-kinase) activity acts to inhibit calcium-dependent chloride secretion in T84 colonic epithelial cells. To further distinguish between the contributions of these two signaling pathways to the inhibition of secretion, we studied effects of insulin, because the insulin receptor links to PI 3-kinase but not to pathways postulated to generate Ins(3,4,5,6)P(4). Chloride secretion across T84 cell monolayers was studied in Ussing chambers. Activation of PI 3-kinase was assessed by Western blotting. Basolateral, but not apical, addition of insulin inhibited carbachol- and thapsigargin-induced chloride secretion in a time- and concentration-dependent fashion. Insulin-like growth factor-I (IGF-I) had similar effects. Insulin had no effect on Ins(3,4,5,6)P(4) levels, and the inhibitory effects of insulin and IGF-I on chloride secretion were fully reversed by the PI 3-kinase inhibitors wortmannin and LY-294002. Western blot analysis showed that both insulin and IGF-I recruited the 85-kDa regulatory and 110-kDa catalytic subunits of PI 3-kinase to anti-phosphotyrosine immunoprecipitates. In conclusion, insulin and IGF-I act to inhibit calcium-dependent chloride secretion through a PI 3-kinase-dependent pathway. Because insulin is released in a pulsatile fashion postprandially and IGF-I levels are elevated in pathological settings, our findings may have physiological and/or pathophysiological significance.

Androstadienes↗
PubMed1983

Drug therapy in resuscitation from electromechanical dissociation.

Electromechanical dissociation (EMD) (organized ECG activity without myocardial contractions) is thought to be rare and associated with poor prognosis. Epinephrine, calcium chloride, and atropine are recommended during attempted resuscitation. Epinephrine's effectiveness in other forms of cardiac arrest is due to its alpha-adrenergic action. Its beta-adrenergic effect may be a disadvantage which is not characteristic of methoxamine, a pure alpha-agonist. Forty anesthetized dogs were asphyxiated until asystolic. Five min later each had slow organized ECG activity. Ventilation with air and sternal compressions were started; 10 dogs each received saline, atropine, calcium chloride, or methoxamine iv. Resuscitation was discontinued after 10 min. Two dogs were resuscitated after saline. Results were not significantly better after atropine or calcium chloride. All 10 which received methoxamine were resuscitated; methoxamine, given at the end of the protocol to all dogs not resuscitated with atropine or calcium chloride, promptly restored spontaneous circulation.

Animals↗
PubMedDate not supplied

Effect of cardiopulmonary bypass and calcium administration on the splanchnic circulation.

Gastrointestinal complications following cardiopulmonary bypass (CPB) are associated with high mortality rates. The identification of prolonged CPB time and calcium administration as independent predictors of gastrointestinal complications suggests decreased splanchnic perfusion as a possible mechanism. To test this hypothesis, we evaluated splanchnic organ perfusion during CPB and after calcium chloride administration. Mongrel dogs were studied under anesthesia and were cannulated for bypass. CPB was begun at 37 degrees C, and the heart was fibrillated and vented. After 30 min, CPB temperature was reduced to 25 degrees C for 1 h with the heart arrested through cold crystalloid cardioplegia. After rewarming to 37 degrees C for 30 min, the heart was cardioverted, and CPB was weaned off. Calcium chloride (10 mg/kg) or saline was administered. Organ blood flow was determined with radiolabeled microspheres at baseline, during CPB, and after weaning from CPB. Splanchnic organ blood flow did not decrease during any phase of CPB. Calcium chloride administration after CPB had no effect on splanchnic organ blood flow. While gastrointestinal injury may result from CPB, this study suggests that the mechanism of injury is not decreased by splanchnic organ perfusion during bypass. While calcium chloride can cause pancreatic injury, the responsible mechanism is not calcium-induced hypoperfusion.

Animals↗