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Food chloride distribution in nature and its relation to sodium content.

Because of growing interest in the biological and clinical effects of dietary chloride as the anion accompanying the dietary cation sodium and because the standard food composition tables used in the United States to estimate sodium content do not contain data on chloride content, we analyzed the nutrient data base of the English workers Paul and Southgate, which contains an extensive listing of both chloride and sodium contents in foods. To examine food chloride distribution in nature, we focused on the uncooked, unadulterated, discrete, primitive foods in the data base (no. = 216 food items). The findings indicate the existence of both a large variability of chloride content among foods and a high degree of coupling of chloride with sodium. The contents of chloride and sodium varied over a similarly large range (coefficients of variation, 229% vs. 263%), differed very little from each other on the average (less than 20%), and correlated (r = 0.84, p less than 0.001) to the extent that greater than two-thirds of the overall variation of chloride content was linked to that of sodium content. Those findings accord with the often posited but untested assertion that the chloride content of foods approximates and parallels that of sodium.(ABSTRACT TRUNCATED AT 250 WORDS)

Chlorides↗

Sodium chloride depletion in a cat with fistulated meningomyelocele.

Decreased serum and CSF chloride concentrations were documented in a 5-year-old Manx cat referred for evaluation of anorexia. Inadequate chloride intake coupled with chloride loss through a fistulated meningomyelocele probably caused chloride deficiency. The inciting cause of anorexia was not determined. The cat was treated with 0.9% NaCl solution. Normal serum and CSF chloride concentrations were restored. Lumbar myelography was performed to delineate the meningocutaneous tract, which then was dissected surgically and was ligated. The cat's body attempted to maintain normal CSF chloride concentration even though the serum chloride concentration was decreased markedly. Calculations made on the basis of rate of CSF production, CSF chloride concentration, and duration of anorexia provided supportive evidence for an active transport system for chloride from plasma to CSF.

Animals↗

Chloride-dependence of the actions of phlorizin on frog skeletal muscle membrane.

The effects of phlorizin on the membrane potential changes induced by cevadine were compared in the presence and absence of external chloride anions in frog skeletal muscle. The action of the drug on 24Na-efflux was also studied in chloride-free medium. In accordance with previous results, it was found that phlorizin reduced the frequency of the membrane potential oscillation (1 mmol/l) or fully inhibited the rhythmic activity (2 mmol/l) in the presence of chloride anions. Replacing the total chloride content of bathing fluid with non-penetrating anions (glutamate, isethionate or sulphate) the inhibitory action of phlorizin on the membrane potential oscillation failed to appear while it reappeared rapidly if the chloride ions were partially restored in the incubating medium. The membrane potential changes evoked by changing the chloride concentration of Ringer solution at constant [K]0 were more expressed in the presence of phlorizin. The action of phlorizin on 24Na-transport proved to be a chloride-independent phenomenon. This finding indicates that the inhibitory effect of phlorizin on Na-transport processes may not be the reason of its blocking action on membrane potential oscillation. Furthermore, it suggests that failure of the drug to inhibit the membrane potential oscillation in the absence of chloride anions may not be accounted for the lack of phlorizin-binding under those circumstances. It is therefore assumed that the increase in chloride conductance may play a causal role in the inhibitory effect of phlorizin on membrane potential oscillation.

Animals↗

Stability and availability of cyclosporine in 5% dextrose injection or 0.9% sodium chloride injection.

The stability of cyclosporine in commonly used i.v. solutions and the percentage of the drug delivered via polyvinyl chloride administration tubing were studied. Cyclosporine injection was prepared according to the manufacturer's instructions and diluted with 5% dextrose injection (D5W) or with 0.9% sodium chloride injection (NS). Admixtures containing cyclosporine 2 mg/mL were prepared in polyvinyl chloride minibags (five for each solution) and in glass containers (three for each solution). The sample obtained at time zero from a glass container protected from light was the control. Additional samples were prepared in minibags and run through 70-inch polyvinyl chloride administration sets. An HPLC assay for cyclosporine was used. Exposure to room light did not significantly affect cyclosporine concentrations. More than 90% of the initial drug concentration remained after 24 hours under all storage conditions, but less than 95% remained after 6 hours in samples diluted with NS and stored in plastic. At times up to 60 minutes, cyclosporine concentrations were significantly different in solutions infused from the minibags through polyvinyl chloride tubing from those in control solutions. Under these conditions, cyclosporine is stable in D5W in glass containers or polyvinyl chloride minibags for 24 hours and in NS for 6 hours (polyvinyl chloride) to 12 hours (glass). However, because of the potential for leaching of plasticizers, cyclosporine admixtures should be stored in glass or used within six hours if stored in polyvinyl chloride minibags. Approximately 10% of the initial drug concentration is lost to 70-inch length polyvinyl chloride infusion tubing.

Adsorption↗

Halide binding by the purified halorhodopsin chromoprotein. II. New chloride-binding sites revealed by 35Cl NMR.

Halorhodopsin is a light-driven chloride pump in the cell membrane of Halobacterium halobium. Recently, a polypeptide of apparent Mr = 20,000 has been purified that contains the halorhodopsin chromophore. Here we use 35Cl NMR to show that the purified chromoprotein possesses two previously unknown classes of chloride-binding sites. One class exhibits a low affinity (KD much greater than 1 M) for chloride and bromide. The second class exhibits a higher affinity (KD = 110 +/- 50 mM) for chloride and also binds other anions according to the affinity series I-, SCN- greater than Br-, NO-3 greater than Cl- greater than F-, citrate. Both classes of NMR site remain intact at pH 11, indicating that the essential positive charges are provided by arginine. Also, both classes are unaffected by bleaching, suggesting that the sites are not in the immediate vicinity of the halorhodopsin chromophore. Although the chromoprotein also appears to contain the chloride-transport site (Steiner, M., Oesterhelt, D., Ariki, M., and Lanyi, J. K. (1984) J. Biol. Chem. 259, 2179-2184), this site was not detected by 35Cl NMR, suggesting that the transport site is in the interior of the protein where it is sampled slowly by chloride in the medium. It is proposed that the purified chromoprotein possesses a channel leading from the medium to the transport site and that the channel contains the high affinity NMR site which facilitates the migration of chloride between the medium and the transport site. We have also used 35Cl NMR to study chloride binding to purified monomeric bacteriorhodopsin; however, this protein contains no detectable chloride-binding sites.

Bacteriorhodopsins↗

ATPo but not cAMPi activates a chloride conductance in mouse ventricular myocytes.

OBJECTIVE: The aim was to test for the presence of cAMPi activated and ATPo activated chloride conductances (ICl(cAMP) and ICl(ATP)) in mouse ventricular myocytes. METHODS: Membrane currents were measured in enzymatically dissociated ventricular myocytes using the whole cell configuration of the patch clamp technique. RESULTS: After inhibiting the activation of sodium, calcium, and potassium currents, increasing [cAMP]i with isoprenaline (1 microM), forskolin (10 microM), or isobutylmethylxanthine (500 microM) had no effect on residual membrane current but extracellular ATP (100 microM) elicited a time independent background conductance. The ATP-activated conductance was observed during voltage steps ranging from +40 to -110 mV from a holding potential of -30 mV within 1 min after adding ATP to the bath. The reversal potential for the ATP activated conductance varied with changes in the chloride gradient and was within several mV of the predicted Nernst potential for chloride. Partially substituting external chloride with aspartate attenuated the ATP activated currents and shifted the reversal potential to values close to those predicted for ECl, suggesting the chloride selective nature of the conductance. The poorly hydrolysable ATP analogue ATP gamma S (100 microM) also elicited the chloride conductance, suggesting purinoceptor linked activation rather than a mechanism dependent on hydrolysis of ATP by ectoATPases. The conductance may be activated following P2 and not P1 purinoceptor stimulation, since the P1 purinoceptor agonists adenosine (500 microM) and adenosine monophosphate (500 microM) had no effect in seven and four cells, respectively. Activation of ICl(ATP) is not likely to be dependent on increased [Ca2+]i since ATP activated the current in cells dialysed with 10 mM EGTA or 20 mM BAPTA. CONCLUSIONS: (1) cAMPi does not activate a chloride conductance in mouse ventricular myocytes; (2) ATPo does activate a chloride conductance, through stimulation of a P2 purinoceptor; and (3) Ca2+i and cAMPi are not involved in activation of ICl(ATP). Also, macroscopic ICl(ATP) from mouse ventricle and ICl(cAMP) from other species appear to be indistinguishable in terms of time independence and rectification properties that depend on the concentration and permeability of intracellular anions. ICl(ATP) could be of physiological and pathophysiological significance considering the ability of chloride channels to modulate cardiac electrical activity and the fact that ATP may be an important neuromediator in the heart.

1-Methyl-3-isobutylxanthine↗

Inadequate measurement of urinary chloride.

Urinary electrolytes are invaluable in the differential diagnosis and treatment of certain acid-base diseases. We have evaluated the accuracy and precision of three different automated chemistry analyzers and a chloridometer (Corning 925 Chloridometer, Hitachi 717 and 917 and Vitros 950) for chloride, sodium and potassium using standard solutions. Data indicate that the ISE modules on the Hitachi 717 and 917 analyzers measure sodium and potassium accurately and precisely throughout the studied concentration range. The Vitros 950 system had the poorest precision and accuracy performance at the low levels of sodium and potassium. The chloride ion-selective membranes on the Hitachi analyzers seriously overestimate the chloride concentration at all levels. The manual dilution method on the Vitros 950 analyzer for chloride measurements showed good precision and accuracy only at the higher chloride levels. For chloride determination the chloridometer displayed the best accuracy with good precision. We recommend that laboratories use chloridometers for the measurement of urinary chloride, and that the CAP include low chloride samples in their proficiency testing program for urine chloride.

Autoanalysis↗

The effects of chloride ions in excitation-contraction coupling and sarcoplasmic reticulum calcium release in twitch muscle fibre.

Using the sucrose vaseline gap technique, experiments were carried out on isolated frog twitch muscle fibre to investigate the role of chloride ions in excitation-contraction coupling. In current clamp conditions, replacement of chloride ions by impermeant anions led to an increase of the amplitude of the early after potential and of the amplitude of the twitch. Addition of a chloride channel blocker, anthracene-9-carboxylic acid gave similar results. In voltage clamp conditions, replacement of chloride ions by impermeant anions induced a decrease of the outward current and an increase of both the amplitude of the contraction and of the resting tension. Addition of anthracene-9-carboxylic acid gave similar results except that resting tension was not modified. Replacement of chloride ions by impermeant anions resulted in a shift of the tension-voltage relationship toward negative potentials and in an increase of the amplitude of the contraction at all potentials. Outward currents were also reduced at all potentials but no shift of the current-voltage relationship was observed. Similar results were obtained upon addition of anthracene-9-carboxylic acid. Rapid filtration experiments were performed on isolated sarcoplasmic reticulum vesicles to study the role of chloride ions in Ca2+ release. Under conditions where KCl was present in the intra- and extravesicular media, removal of chloride ions from the release solution produced a 2-fold increase in the rate of Ca(2+)-induced Ca2+ release. Together, these results suggest that, besides their involvement in the action potential time course, chloride ions could exert a negative control on the sarcoplasmic reticulum Ca2+ release.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗

Metabolism of chloride in halophilic prokaryotes.

While much understanding has been achieved on the intracellular sodium and potassium concentrations of halophilic and halotolerant microorganisms and on their regulation, we know little on the metabolism of anions. Archaea of the family Halobacteriaceae contain molar concentrations of chloride, which is pumped into the cells by cotransport with sodium ions and/or using the light-driven primary chloride pump halorhodopsin. Most halophilic and halotolerant representatives of the bacterial domain contain low intracellular ion concentrations, with organic osmotic solutes providing osmotic balance. However, some species show a specific requirement for chloride. In Halobacillus halophilus certain functions, such as growth, endospore germination, motility and flagellar synthesis, and glycine betaine transport are chloride dependent. In this organism the expression of a large number of proteins is chloride regulated. Other moderately halophilic Bacteria such as Halomonas elongata do not show a specific demand for chloride. A very high requirement for chloride was demonstrated in two groups of Bacteria that accumulate inorganic salts intracellularly rather than using organic osmotic solutes: the anaerobic Halanaerobiales and the aerobic extremely halophilic Salinibacter ruber. It is thus becoming increasingly clear that chloride has specific functions in haloadaptation in different groups of halophilic microorganisms.

Bacillaceae↗

A Novel voltage-dependent chloride current activated by extracellular acidic pH in cultured rat Sertoli cells.

Sertoli cells from mammalian testis are key cells involved in development and maintenance of stem cell spermatogonia as well as secretion of a chloride- and potassium-rich fluid into the lumen of seminiferous tubules. Using whole-cell patch clamp experiments, a novel chloride current was identified. It is activated only in the presence of an extracellular acidic pH, with an estimated half-maximal activation at pH 5.5. The current is strongly outwardly rectifying, activated with a fast time-dependent onset of activation but a slow time-dependent kinetic at depolarization pulses. The pH-activated chloride current was not detected at physiological or basic pH and is not sensitive to intracellular or extracellular Ca2+ variation. Diphenylamine-2-carboxylic acid and 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid blocked the induced currents, and its anionic selectivity sequence was Cl- > Br- > I-> gluconate. We have performed a reverse transcription-PCR analysis to search for voltage-dependent chloride rClC channels in cultured rat Sertoli cells. Among the nine members of the family only rClC-2, rClC-3, rClC-6, and rClC-7 have been identified. The inwardly rectifying rClC-2 chloride current was activated by hyperpolarization but not by pH variation. A different depolarization-activated outwardly rectifying chloride current was activated only by hypotonic challenge and may correspond either to rClC-3 or rClC-6. Immunolocalization experiments demonstrate that rClC-7 resides in the intracellular compartment of Sertoli cells. This study provides the first functional identification of a native acid-activated chloride current. Based on our molecular analysis of rClC proteins, this new chloride current does not correspond to rClC-2, rClC-3, rClC-6, or rClC-7 channels. The potential physiological role of this native current in an epithelial cell from the reproductive system is discussed.

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

Chloride dependence of endospore germination in halobacillus halophilus

The ion requirement for germination and outgrowth of endospores from the moderately halophilic salt marsh bacterium Halobacillus halophilus was studied. Germination and outgrowth of endospores plated onto nutrient broth was dependent on the salt concentration in the artificial seawater used as the source of ions. Maximal germination and outgrowth were observed when double-concentrated artificial seawater was used. Replacement of chloride salts in the artificial seawater by other salts resulted in a complete loss of germination and outgrowth that was restored upon addition of chloride. To analyze the role of chloride more directly and quantitatively, a defined growth medium was used in which the artificial seawater was substituted by a solution of magnesium sulfate and sodium chloride. Spore germination and outgrowth were strictly dependent on the chloride concentration; maximal germination and outgrowth were observed at approximately 1.3 M Cl(-). Chloride could be substituted by bromide, but not by sulfate or nitrate. Microscopic examinations of single spores clearly showed that germination is the chloride-dependent step. This first report on chloride dependence of spore germination in any endospore-forming bacterium adds another function to chloride in H. halophilus apart from its being essential for the physiology of the vegetative cell. http://link.springer. de/link/service/journals/00203/bibs/9172004/91720264.htm</HEA

Journal Article↗

Toxicity of triorganotin compounds: comparative in vivo studies with a series of trialkyltin compounds and triphenyltin chloride in male rats.

In 2-week feeding studies, a series of trialkyltin chlorides and triphenyltin chloride were fed to male weanling rats at different dietary concentrations to evaluate their toxic effects, especially on the brains and the lymphoid organs, thymus and spleen. The lower trialkyltin homologs, trimethyltin chloride (TMTC) and triethyltin chloride (TETC), were neurotoxic, causing neuronal degradation and cerebral edema, respectively, at dietary concentrations of 15 ppm. The intermediate homologs, tri-n-propyltin chloride (TPTC) and tri-n-butyltin chloride (TBTC), and the aromatic compound, triphenyltin chloride (TPhTC), caused a dose-related reduction of thymus weight. At a dietary concentration of 150 ppm decreases in thymus weight to 53, 39, and 81% of controls were found following treatment with TPTC, TBTC, and TPhTC, respectively. Microscopically, thymus atrophy was associated with a lymphocyte depletion in the thymic cortex. Only 16% of the total number of nucleated thymocytes could be isolated from rats fed 150 ppm TBTC. These effects were completely reversed within 2 weeks. Slight thymus atrophy was observed after feeding a relatively high dose of 150 mg tri-n-hexyltin chloride (THTC)/kg diet, whereas tri-n-octyltin chloride (TOTC) was ineffective. A dose-related decrease in spleen weight was noticed after 2 weeks feeding of TPTC, TBTC, and TPhTC. Liver weights were increased in rats fed TBTC, THTC, and TPhTC for 2 weeks. Nevertheless, no enlarged livers and normal spleen weights were found upon feeding 100 ppm TPTC or TBTC for 4 weeks, whereas thymus weight was severely decreased. Therefore, atrophy of the thymus was considered to be the predominant effect of the intermediate trialkyltins (TPTC, TBTC). From this study it is concluded that the lower trialkyltins (TMTC, TETC) are essentially neurotoxic, the intermediate trialkytins (TPTC, TBTC) and triphenyltin are primarily immunotoxic, and the higher homologs (THTC, TOTC) are only slightly toxic or not toxic at all.

Administration, Oral↗

Effect of nickel chloride on body temperature and behavioral thermoregulation in the rat.

This study was designed to assess the effects of acute nickel chloride administration on behavioral and autonomic thermoregulation in the rat. In one experiment, male rats of the Fischer 344 strain were injected with nickel chloride (IP) at dosages of 0 to 24.0 mg/kg and placed in an environmental chamber maintained at an ambient temperature (Ta) of 10 or 20 degrees C. Colonic temperature was measured 60 min postinjection. Nickel chloride caused a dose-related decrease in colonic temperature, and the hypothermia was accentuated at the cooler Ta. In a second study, rats injected with 0, 6.0, 12.0, or 24.0 mg/kg nickel chloride were placed in a temperature gradient which allowed the rats to select their preferred thermal environment. Nickel chloride at dosages of 12.0 and 24.0 mg/kg caused a significant reduction in the selected Ta. At these dosages the rats were also significantly hypothermic at 60 min postinjection. In a third experiment, whole-body oxygen consumption (i.e., metabolic rate) was measured at Ta's of 10, 20, and 30 degrees C following a 12.0 mg/kg injection of nickel chloride. Nickel chloride caused an initial depression in metabolic rate and hypothermia at Ta's of 10 and 20 degrees C but not at 30 degrees C. In conclusion, (a) nickel chloride affects both behavioral and autonomic control of thermoregulation in the rat and appears to induce a regulated decrease in body temperature and (b) the behavioral thermoregulatory response of the rat is less sensitive to nickel chloride when compared to the mouse.

Animals↗

Effects of multiple applications of benzalkonium chloride and nonoxynol 9 on the vaginal epithelium in the pigtailed macaque (Macaca nemestrina).

OBJECTIVE: Safe and effective vaginally applied microbicides could help to control the continuing spread of sexually transmitted diseases. STUDY DESIGN: This study used nonhuman primates to test the effects of multiple applications of nonoxynol 9, benzalkonium chloride, or a combination on vaginal flora and lower reproductive tract tissues. Fourteen monkeys (Macaca nemestrina) received daily vaginal applications of nonoxynol 9, benzalkonium chloride, or both for 3 to 4 days. Vaginal microflora and colposcopic observations were made at baseline and during and after completion of treatments. Cervical biopsy specimens were collected from a subset of animals. RESULTS: Cervical erythema and vaginal erythema were observed in all 3 treatment groups. Cervical papillae and epithelial disruption were present in both the nonoxynol 9 and the nonoxynol 9 plus benzalkonium chloride groups. Vaginal epithelial disruption was noted in both the benzalkonium chloride and the nonoxynol 9 plus benzalkonium chloride groups. Cervical biopsy specimens from each group revealed acute inflammatory infiltrates with occasional plasma cells and lymphoid follicles. Detection of most microorganisms, including viridans streptococci, decreased in the benzalkonium chloride and the nonoxynol 9 plus benzalkonium chloride groups. Detection of Lactobacillus species decreased in the benzalkonium chloride group. All microflora levels recovered after several days without microbicide use. CONCLUSIONS: Although nonoxynol 9 is currently the only microbicide approved for use as a spermicide in the United States, its repeated use may be detrimental to the epithelial tissues of the female reproductive tract. Benzalkonium chloride, currently approved for use in other countries, not only may damage epithelial tissues but also appears to reduce the population of potentially protective Lactobacillus species in the vagina.

Animals↗

Submicrometric lipobead-based fluorescence sensors for chloride ion measurements in aqueous solution.

This paper describes the preparation and optimization of the analytical properties of fluorescence-based submicrometric chloride ion sensing lipobeads. Fluorescence sensing lipobeads are polystyrene nanoparticles that are coated with a phospholipid membrane that contains a fluorescent indicator for a targeted analyte. In this study, the halide-specific fluorescence dye, lucigenin, was immobilized into the phospholipid membrane of the lipobeads to enable chloride ion detection. The fluorescence intensity of lucigenin decreases with increasing chloride ion concentration due to dynamic quenching. Lipobeads that contained only lucigenin were ineffective as chloride ion sensors due to poor partition of the water-soluble lucigenin molecules into the phospholipid membrane and high leakage rate of immobilized lucigenin molecules to the aqueous solution. To stabilize the chloride ion sensing lipobeads we coimmobilized hexadecanesulfonate molecules into the phospholipid membrane. The formation of ion pairs between hexadecanesulfonate and lucigenin decreased the hydrophilicity of the dye, increased its partition rate into the membrane, increased the brightness of the particles, and significantly decreased the leakage rate of the hydrophobic ion pair from the membrane to the solution. To further improve their chloride ion sensitivity, we also immobilized the chloride ionophore [9] mercuracarborand-3 into the lipobead membrane. The study resulted in a unique submicrometric chloride ion sensor, which is suitable for chloride ion measurements in biological fluids.

Journal Article↗

The contribution of histamine release to bronchoconstriction provoked by inhaled benzalkonium chloride in asthma.

1. To investigate the possibility that benzalkonium chloride-induced bronchoconstriction results from the endogenous release of histamine, we examined the effect of the selective histamine antagonists terfenadine and astemizole, on the airways response to inhaled benzalkonium chloride and histamine in 12 asthmatic subjects. 2. Double-blind concentration- and time-course studies were undertaken, 3 h after treatment with terfenadine or matched placebo. 3. Benzalkonium chloride and histamine caused concentration-related falls in FEV1 in all subjects with benzalkonium chloride being 7.4 times less potent as a bronchoconstrictor agonist than histamine. Terfenadine displaced to the right the benzalkonium chloride and histamine concentration-response curves by 3.7 and 111 fold respectively. Terfenadine attenuated the initial (5 min) bronchoconstrictor response to benzalkonium chloride by 40%. However, over the whole 45 min period, the response was reduced by only 13% compared with 86% inhibition of the response to histamine. 4. In an open study, eight of the 12 subjects undertook a time course study with inhaled benzalkonium chloride after pretreatment with the chemically unrelated histamine antagonist astemizole. Astemizole inhibited benzalkonium chloride-induced bronchoconstriction to an almost identical degree as that achieved with terfenadine. 5. We conclude that the initial bronchoconstrictor effect of benzalkonium chloride is due, in part, to histamine release. However, the majority of the adverse effect relates to other, as yet unrecognised effects of this bacteriocidal substance.

Adult↗

Immediate effect of benzalkonium chloride in decongestant nasal spray on the human nasal mucosal temperature.

Benzalkonium chloride is a preservative commonly used in nasal decongestant sprays. It has been suggested that benzalkonium chloride may be harmful to the nasal mucosa. Decongestion with the vasoconstrictor xylometazoline containing benzalkonium chloride has been shown to cause a significant reduction of the nasal mucosal temperature. The purpose of the present study was to determine the short-term influence of xylometazoline nasal spray with and without benzalkonium chloride on the nasal mucosal temperature. Healthy volunteers (30) were included in the study. Fifteen volunteers received xylometazoline nasal spray (1.0 mg/mL) containing benzalkonium chloride (0.1 mg/mL) and 15 age-matched subjects, received xylometazoline nasal spray without benzalkonium chloride. Using a miniaturized thermocouple the septal mucosal temperature was continuously measured at defined intranasal detection sites before and after application of the nasal spray. The mucosal temperature values did not significantly differ between the group receiving xylometazoline containing benzalkonium chloride and the group receiving xylometazoline spray without benzalkonium chloride before and after decongestion (P > 0.05). In both study groups septal mucosal temperatures significantly decreased after decongestion (P < 0.05) because of a reduction of the nasal mucosal blood flow following vasoconstriction. This study indicates that benzalkonium chloride itself does not seem to influence nasal blood flow and nasal mucosal temperature in topical nasal decongestants.

Administration, Inhalation↗

Allergic patch test reactions to palladium chloride in schoolchildren.

A study of the prevalence of allergic patch test reactions to palladium chloride compared to nickel sulfate was performed in a group of Finnish schoolchildren. All adolescents 14-18 years of age in a Finnish town with 40,000 inhabitants, who had received orthodontic treatment with metallic appliances at a municipal dental clinic, were included in the study. The selection of patients was based on patient records. A non-treatment control group was randomly selected from the same age groups of the town population. A total of 700 subjects (77% of those invited), 417 (60%) girls and 283 (40%) boys, participated. The majority (91%) of the girls had pierced ears. Orthodontic treatment was equally common (67-70%) in the boys and the girls. The girls had a much higher frequency of allergic patch test reactions to both nickel sulfate and palladium chloride. Of the 700 adolescents tested, 48 (7%) had an allergic patch test reaction to palladium chloride. Of the 417 girls, 44 (11%) were palladium-chloride-positive, whereas only 4 of the 283 boys tested (1%) had an allergic patch test reaction to palladium chloride. 3 patients reacted to palladium chloride only, whereas all other patients with allergic patch test reactions to palladium chloride also had an allergic patch test reaction to nickel sulfate. The results support the concept of cross-reactivity between nickel sulfate and palladium chloride. The clinical significance of the allergic patch test reactions caused by palladium chloride remains unclear.

Adolescent↗