Search PubMed⌕ Search

SEARCH · Search PubMed

Results for “Sodium Compounds”

Search indexed PubMed citations on genomics, clinical trials, systematic reviews and public health. Explore titles, authors and supplied subject terms, then open the PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 307 records · Page 17Linked to original sources
PubMed1985

Histamine and leukotriene-independent guinea-pig anaphylactic shock unaccounted for by Paf-acether.

Ovalbumin induced dose-dependent contractions of lung parenchyma strips from sensitized guinea-pigs, whereas Paf-acether (1-alkyl-2-acetyl-sn-glycero-3-phosphoryl choline), a potential mediator of immediate hypersensitivity, induced a single contraction, followed by specific desensitization to a second exposure. Lung strips desensitized to Paf-acether contracted to ovalbumin as did non-desensitized controls, even in the presence of inhibitors of other mediators of anaphylaxis. Contractions by Paf-acether and by ovalbumin were reduced by nordihydroguaiaretic acid (NDGA) and by the phospholipase A2 inhibitor p-bromophenacyl bromide (0.1-0.3 mM). Three other anti-lipoxygenase agents (diethylcarbamazine, 5 mM; eicosatetraynoic acid and BW755c, 0.1 mM), reduced the contractions by ovalbumin but also those due to acetylcholine, indicating non-specific effects. Neither the anti-allergic compound sodium cromoglycate (3 mM) nor the anti-leukotriene agent, FPL 55712 (0.01 mM), inhibited the contractions by ovalbumin or by Paf-acether. A sensitized strip stimulated with ovalbumin released substances which contracted a non-sensitized strip mounted in the same organ bath. The contractions of the non-sensitized strip were abolished by FPL 55712 (0.01 mM), by NDGA and BW755c, (0.1 mM), whereas those of the sensitized one were unaffected. Leukotrienes are formed by the lung strips during shock but alone, they do not explain the contractile activity. The intravenous administration of ovalbumin (1 mg kg-1) led to bronchoconstriction and thrombocytopenia, which were not modified by the anti-leukotriene substance FPL 55712 nor by aspirin. Bronchoconstriction was suppressed if FPL 55712 was used in combination with aspirin (20 mg kg-1), mepyramine and methysergide (200 micrograms kg-1 of either). Pretreatment of the guinea-pigs with propranolol reduced this inhibition to approximately 60%. In no instance was thrombocytopenia prevented. In vitro contractions of the actively sensitized lung strip are not fully accounted for by histamine, FPL 55712-inhibitable leukotrienes or Paf-acether, whereas in systemic anaphylaxis histamine and leukotrienes (inhibited respectively by mepyramine and by FPL 55712) have a significant role.

Acetophenones↗
PubMed1988

Expression of heat stress proteins by human periodontal ligament cells.

The purpose of the present report was to document the stress response produced by physical and chemical abuses to human periodontal ligament cells, and to review some of the known functions of stress response proteins produced as a result of such treatments. For these studies human PDL cells were exposed to sublethal challenges of 43 degrees C heat, sodium arsenite and the amino acid analog L-azetidine-2-carboxylic acid (AZC). The cells were labelled with [35S]-methionine and the proteins produced were examined by autofluorography of SDS-PAGE gels. Heat challenges were shown to induce hsps with an apparent mol. wts. of 90K, 68-72K, 41-47K, and 36 K. Arsenite-treated cells produced similar hsps including a 30k protein not produced by other forms of stress. AZC treatment resulted in the production of apparent functionless hsps with apparent molecular weights of 90,000, 72,000, 68,000 and 36,000. The function of these proteins and their possible role in periodontal disease is discussed.

Arsenic↗
PubMed2004

Nitric oxide is toxic to melanocytes in vitro.

Nitric oxide is a diffusible gaseous mediator generated from l-arginine by inducible and constitutive nitric oxide synthases. It has been associated with cytotoxic effects. Inflammatory cells and Langerhans cells can express the inducible form of nitric oxide synthase and produce large quantities of nitric oxide. The proximity of these cells to melanocytes could result in melanocyte cell death. We studied melanocyte susceptibility to nitric oxide using the nitric oxide donor compound sodium nitroprusside and nitric oxide released by the Langerhans like cell-line XS-52 following stimulation with lipopolysaccharide (LPS). Melanocyte lysis, quantified by chromium release in the presence of sodium nitroprusside was both time and concentration dependent. Co-culture of LPS-stimulated XS cells with melanocytes also resulted in melanocyte cell death. No cell death was observed when melanocytes alone were exposed to LPS. Melanocytes were killed even when the co-cultures were performed across Transwells in which there was no direct contact between XS cells and melanocytes. XS-induced melanocyte death was thus dependent on a diffusible factor consistent with nitric oxide. Cell death was markedly decreased in co-cultures performed in the presence of hemoglobin, a nitric oxide quencher. The possible role that nitric oxide may play in disorders associated with loss of pigmentation is discussed.

Animals↗
PubMed2002

Dominance of pressure natriuresis in acute depressor responses to increased renal artery pressure in rabbits and rats.

Increasing renal artery pressure (RAP) activates pressure diuresis/natriuresis and inhibits renal renin release. There is also evidence that increasing RAP stimulates release of a putative depressor hormone from the renal medulla, although this hypothesis remains controversial. We examined the relative roles of these antihypertensive mechanisms in the acute depressor responses to increased RAP in anaesthetized rabbits and rats. In rabbits, an extracorporeal circuit was established which allows RAP to be set and controlled without direct effects on systemic haemodynamics. When RAP was maintained at approximately 65 mmHg, cardiac output (CO) and mean arterial pressure (MAP) did not change significantly. In contrast, when RAP was increased to approximately 160 mmHg, CO and MAP fell 20 +/- 5 % and 36 +/- 5 %, respectively, over 30 min. Urine flow also increased more than 28-fold when RAP was increased. When compound sodium lactate was infused intravenously at a rate equal to urine flow, neither CO nor MAP fell significantly in response to increased RAP. In 1 kidney-1 clip hypertensive rats, MAP fell by 54 +/- 10 mmHg over a 2 h period after unclipping. In rats in which isotonic NaCl was administered intravenously at a rate equal to urine flow, MAP did not change significantly after unclipping (-14 +/- 9 mmHg). Our results suggest that the depressor responses to increasing RAP in these experimental models are chiefly attributable to hypovolaemia secondary to pressure diuresis/natruresis. These models therefore appear not to be bioassays for release of a putative renal medullary depressor hormone.

Animals↗
PubMed1995

Endotoxin-induced desensitization of mouse macrophages is mediated in part by nitric oxide production.

Refractoriness (tolerance) to endotoxin effects, such as induction of tumor necrosis factor alpha (TNF-alpha) secretion, can be elicited in vitro in macrophages by preexposure of cells to endotoxin (lipopolysaccharide [LPS]) itself. The aim of this study was to determine whether this phenomenon is due to negative feedback mediated by the free radical nitric oxide (NO) produced by cells when they are activated by LPS. Among several efficient inhibitors of NO production, NG-monomethyl-L-arginine did not induce concomitant inhibition of TNF-alpha secretion. Mouse macrophages that were exposed to LPS in the presence of NG-monomethyl-L-arginine partially maintained the ability to secrete TNF-alpha in response to a second LPS stimulation, compared with cells preexposed to LPS alone, thus suggesting that NO is involved in part in LPS-induced desensitization of cells. Furthermore, direct exposure of cells to the NO-generating compounds sodium nitroprusside and S-nitroso-N-acetylpenicillamine mimicked LPS-induced desensitization. However, low concentrations of a synthetic lipid (lipid M4) that is structurally analogous to the reducing end of the lipid A moiety of LPS induced desensitization of mouse macrophages without concomitant production of NO. Taken together, these data suggest that although NO actually takes part in LPS-induced desensitization of mouse macrophages, additional and yet unknown mechanisms must also exist.

Animals↗
PubMed1972

Nutritional studies of Rickettsia guintana: nature of the hematin requirement.

Rickettsia quintana grew in a liquid medium consisting of a brain-heart infusion base supplemented with starch and hematin. The growth requirement for hematin could not be substituted by compounds of known catalytic activity for H(2)O(2), viz., catalase, potassium pyruvate, or charcoal, or by the reducing compounds sodium sulfite and sodium thioglycollate. R. quintana was catalase-negative, but no H(2)O(2) production could be demonstrated by the catalase-aminotriazole technique. A minimum inoculum giving 10(5) cells/ml was required to initiate growth. The generation time at 33 C was 10 hr. The temperature range for growth was 28 to 37 C. Growth was enhanced when succinate or glutamate was added as energy source.

Catalase↗
PubMed2000

Nitric oxide synthesis enhances human immunodeficiency virus replication in primary human macrophages.

Macrophages are suspected to play a major role in human immunodeficiency virus (HIV) infection pathogenesis, not only by their contribution to virus dissemination and persistence in the host but also through the dysregulation of immune functions. The production of NO, a highly reactive free radical, is thought to act as an important component of the host immune response in several viral infections. The aim of this study was to evaluate the effects of HIV type 1 (HIV-1) Ba-L replication on inducible nitric oxide synthase (iNOS) mRNA expression in primary cultures of human monocyte-derived macrophages (MDM) and then examine the effects of NO production on the level of HIV-1 replication. Significant induction of the iNOS gene was observed in cultured MDM concomitantly with the peak of virus replication. However, this induction was not accompanied by a measurable production of NO, suggesting a weak synthesis of NO. Surprisingly, exposure to low concentrations of a NO-generating compound (sodium nitroprusside) and L-arginine, the natural substrate of iNOS, results in a significant increase in HIV replication. Accordingly, reduction of L-arginine bioavailability after addition of arginase to the medium significantly reduced HIV replication. The specific involvement of NO was further demonstrated by a dose-dependent inhibition of viral replication that was observed in infected macrophages exposed to N(G)-monomethyl L-arginine and N(G)-nitro-L-arginine methyl ester (L-NAME), two inhibitors of the iNOS. Moreover, an excess of L-arginine reversed the addition of L-NAME, confirming that an arginine-dependent mechanism is involved. Finally, inhibitory effects of hemoglobin which can trap free NO in culture supernatants and in biological fluids in vivo confirmed that endogenously produced NO could interfere with HIV replication in human macrophages.

Cells, Cultured↗
PubMed1990

Calcium and phosphorus solubility in neonatal intravenous feeding solutions.

The limited solubility of calcium and phosphorus in standard parenteral nutrition formulations has restricted the ability to provide sufficient minerals to preterm infants to prevent substrate deficient metabolic bone disease. We determined the solubility limits of calcium and phosphorus in a total of 160 formulations under carefully controlled conditions. By increasing the concentrations of dextrose, amino acids, and by using Addiphos instead of 8.7% dipotassium hydrogen phosphate as the phosphorus source, higher concentrations of both calcium and phosphorus were held in solution. This should permit the delivery of increased concentrations of these minerals at rates which approximate fetal accretion.

Amino Acids↗
PubMed1990

Acid-base state of the preterm infant and the formulation of intravenous feeding solutions.

An acidic intravenous source of phosphorus (Addiphos) was compared with dipotassium hydrogen phosphate in 25 preterm infants to study acid-base state. Eight infants were given either Addiphos or dipotassium hydrogen phosphate alternately for 48 hour periods and similar amounts of calcium and phosphorus were delivered. There were no significant differences in calcium and phosphorus intake, calcium and phosphate plasma concentrations, or acid-base state between study periods on the two solutions. Seventeen infants were given the two solutions alternately for 72 hour periods; Addiphos was used to increase the amounts of calcium and phosphorus being delivered. Calcium and phosphorus intake was decreased on dipotassium hydrogen phosphate, but Addiphos significantly increased calcium and phosphorus intake and plasma calcium and phosphate concentrations. It also lowered the pH of the urine and raised the titratable acidity. Acid-base state, however, was not significantly different. It is therefore possible to increase intake of calcium and phosphorus in preterm infants without causing a significant metabolic acidosis.

Acid-Base Equilibrium↗
PubMed1986

Chalk in the prime.

After observations of cloudiness in the perfusion circuit at open intracardiac operations, laboratory experiments showed a precipitate in a Hartmann's solution (compound sodium lactate solution, Ringer-lactate) and sodium bicarbonate based priming fluid used for cardiopulmonary bypass. The precipitate was found to consist of calcium carbonate crystals. The crystals were not dissolved by adding plasma proteins, nor were they sufficiently cleared from the extracorporeal circuit by a 40 microns filter in the arterial line. The crystals may embolise in microvascular beds and thus be a cause of postoperative morbidity. The practice of adding sodium bicarbonate to the pump prime may be unnecessary.

Bicarbonates↗
PubMed1983

Work in progress: reduction of calcium activity by radiopaque contrast media.

An in vitro examination of the effects of radiopaque contrast media anions, cations, additives, and ionic strength on ionic calcium level using ion-specific electrodes was made. The calcium-binding additives sodium citrate and sodium EDTA produced the largest reduction in ionic calcium. At the same iodine concentration the anions diatrizoate, iothalamate, metrizoate, and ioxaglate reduced ionic calcium by essentially the same amount. Sodium compounds reduced ionic calcium more than did meglumine compounds, a difference that is probably related to dissociation. The nonionic compounds iohexol and iopamidol did not reduce ionic calcium significantly. Ionic strength appears to have little direct effect on ionic calcium at and above physiologic levels. All ionic contrast media bind significant amounts of ionic calcium at the high concentrations achieved during selective arteriography. Since the anions are only weak calcium binders supplemental calcium can restore the level of ionic calcium.

Angiography↗
PubMed1992

The iodide channel of the thyroid: a plasma membrane vesicle study.

The uptake of radioactive iodide or chloride by plasma membrane vesicles of bovine thyroid was studied by a rapid filtration technique. A Na(+)-I- cotransport was demonstrated. When this Na(+)-I- cotransport is inactive (i.e., at 4 degrees C and in the absence of Na+), an uptake of iodide above chemical equilibrium could be induced, driven by the membrane potential. The latter was set up by allowing potassium to diffuse into the membrane vesicles in the presence of valinomycin and of an inward K+ gradient. This potential difference (positive inside) induced the uptake of iodide (or other anion present). The data support the existence of two anionic channels. The first one, observed at low near-physiological iodide concentration (micromolar range), which exhibits a high permeability and specificity for iodide (hence called the iodide channel), has a Km of 70 microM. The other one appears similar to the epithelial anion channel as described by Landry et al. (J. Gen. Physiol. 90: 779-798, 1987); it is still about fourfold more permeable to iodide than to chloride and presents a Km of 33 mM. Under physiological conditions the latter channel would mediate chloride transport, and the iodide channel, which is proposed to be restricted to the apical plasma membrane domain of the thyrocyte, transports iodide from the cytosol to the colloid space.

Animals↗
PubMed1992

Interactions of endothelins and EDRF in bovine native endothelial cells: selective effects of endothelin-3.

The tone of vascular smooth muscle is influenced by factors released from the endothelium, including endothelin (ET)-1 and endothelium-derived relaxing factor (EDRF). To better understand the interactions between these two mediators, we examined the release of both immunoreactive ET-1 (ir-ET-1) and EDRF from bovine aortic intact endothelium. Bovine aortas were opened longitudinally, washed, and clamped with the endothelium uppermost between two plates. The upper plate contained six openings forming identical and independent wells of endothelial cell monolayer. In experiments examining the release of EDRF, measured as accumulated NO2- and NO3- (NO chi -), we found that ET-3, calcium ionophore A23187 (A23187), acetylcholine (ACh), or ADP caused significant increase in NO chi- release, whereas ET-1 did not. These were significantly reduced in the presence of the EDRF/NO synthase inhibitor, NG-methyl-L-arginine (L-NMA). In a parallel series of experiments measuring EDRF release by stimulation of guanosine 3',5'-cyclic monophosphate (cGMP) accumulation in rat fetal lung (RFL)-6 cells, ET-3 but not ET-1 was also found to be active as a releaser of EDRF. A23187 caused an increase of ir-ET-1 release, whereas ACh, ADP, or the NO-containing compound sodium nitroprusside decreased the release of ir-ET-1. The depression in ir-ET-1 release in the presence of ACh or ADP was not seen when the endothelium was treated with L-NMA. When the cells were pretreated with 8-bromoguanosine 3',5'-cyclic monophosphate (8-bromo-cGMP), the release of ir-ET-1 in response to A23187 was significantly depressed.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed2000

Endothelium modulates anion channel-dependent aortic contractions to iodide.

Anion currents contribute to vascular smooth muscle (VSM) membrane potential. The substitution of extracellular chloride (Cl) with iodide (I) or bromide (Br) initially inhibited and then potentiated isometric contractile responses of rat aortic rings to norepinephrine. Anion substitution alone produced a small relaxation, which occurred despite a lack of active tone and minimal subsequent contraction of endothelium-intact rings (4.2 +/- 1.2% of the response to 90 mM KCl). Endothelium-denuded rings underwent a similar initial relaxation but then contracted vigorously (I > Br). Responses to 130 mM I (93.7 +/- 1.9% of 90 mM KCl) were inhibited by nifedipine (10(-6) M), niflumic acid (10(-5) M), tamoxifen (10(-5) M), DIDS (10(-4) M), and HCO(-)(3)-free buffer (HEPES 10 mM) but not by bumetanide (10(-5) M). Intact rings treated with N(omega)-nitro-L-arginine (10(-4) M) responded weakly to I (15.5 +/- 2.1% of 90 mM KCl), whereas hemoglobin (10(-5) M), indomethacin (10(-6) M), 17-octadecynoic acid (10(-5) M), and 1H-[1,2, 4]oxadiazole[4,3-a]quinoxalin-1-one (10(-6) M) all failed to augment the response of intact rings to I. We hypothesize that VSM takes up I primarily via an anion exchanger. Subsequent I efflux through anion channels having a selectivity of I > Br > Cl produces depolarization. In endothelium-denuded or agonist-stimulated vessels, this current is sufficient to activate voltage-dependent calcium channels and cause contraction. Neither nitric oxide nor prostaglandins are the primary endothelial modulator of these anion channels. If they are regulated by an endothelium-dependent hyperpolarizing factor it is not a cytochrome P-450 metabolite.

Animals↗
PubMed1993

cAMP regulates soluble guanylate cyclase beta 1-subunit gene expression in RFL-6 rat fetal lung fibroblasts.

Endothelium-derived relaxing factor (EDRF)/nitric oxide (NO) activates soluble guanylate cyclase, thereby stimulating the synthesis of guanosine 3',5'-cyclic monophosphate (cGMP). To investigate the regulation of this important EDRF/NO receptor, we studied soluble guanylate cyclase gene expression in a rat fetal lung fibroblast cell line (RFL-6). 3-Isobutyl-1-methylxanthine, forskolin, and dibutyryl adenosine 3',5'-cyclic monophosphate (cAMP), agents which increase intracellular cAMP, decreased the concentration of mRNA encoding the beta 1-subunit of soluble guanylate cyclase in RFL-6 cells. To investigate whether a decrease in beta 1-subunit mRNA concentration was reflected in diminished capacity to produce cGMP, forskolin-treated RFL-6 cells were exposed to the NO-donor compound sodium nitroprusside. Exposure to forskolin reversibly reduced the ability of RFL-6 cells to increase cGMP in response to NO. These observations suggest that cAMP can modulate the cellular response to EDRF/NO by decreasing the expression of one of the subunits of soluble guanylate cyclase.

1-Methyl-3-isobutylxanthine↗
PubMedDate not supplied

Ifosfamide and mesna: effects on the Na/H exchanger activity in renal epithelial cells in culture (LLC-PK1).

Ifosfamide (IF) is an alkylating cytostatic with urotoxic and tubulotoxic side effects which may result in the development of Fanconi syndrome in children. While the urotoxicity of IF is effectively prevented by the uroprotective thiol compound sodium-2-mercaptoethanesulfonate (Mesna), tubulo-toxicity of IF may occur even in the presence of Mesna and in the absence of any signs of urotoxicity. Using the renal tubular cell line LLC-PK1, we investigated whether there is a protective effect of Mesna or of its major dimeric metabolite Dimesna against metabolites of IF with respect to the Na/H exchanger activity. We tested the major IF metabolites 4-hydroperoxy-IF (4-OOH-IF), chloroacetaldehyde (CAA), and acrolein. All metabolites significantly inhibit the Na/H exchanger activity. Half-maximal inhibition of transport occurs at concentrations of 120 mumol/l (4-OOH-IF), 80 (CAA), and 60 mumol/l (acrolein) after 2 h of incubation. The onset of the inhibitory effect of all three metabolites is rapid. Complete inhibition of Na/H exchange by acrolein and CAA is present after a 6-hour exposure to 100 mumol/l of the respective metabolite, while 100 mumol/l 4-OOH-IF causes only 50% inhibition after 24 h of incubation. Dimesna, which the proximal tubular cell has to reduce to Mesna at the expense of intracellular glutathione before it exerts a uroprotective effect, has no protective effect in LLC-PK1 cells. Dimesna (0.3 mmol/l) displaces the dose-response curve for acrolein to the left, indicating an increased toxicity of the combination of acrolein plus Dimesna. Mesna (0.3 mmol/l) has a complete protective effect with respect to acrolein and CAA, while the protective effect versus 100 mumol/l of 4-OOH-IF is incomplete. We conclude that the function of the Na/H exchanger in LLC-PK1 cells is altered by metabolites of IF. The incomplete protection against the toxic effect of 4-OOH-IF by Mesna may explain the pathomechanism by which IF causes tubulotoxicity in the absence of urotoxicity.

Acetaldehyde↗
PubMed1996

Anion translocation through the enamel organ.

The objective of this study was to determine whether cells of the secretory- and maturation-stage enamel organ of rats contain anion translocation mechanisms similar to those found in other ion-regulating epithelia. Sodium bromide (Br) was used to localize the distribution of anions in the enamel organ. Furosemide, an inhibitor of the Na-K-2Cl co-transporter and other anion transporters, was administered with NaBr or sodium fluoride (F) to investigate if halogens other than Cl can use these transport mechanisms. We obtained the data by using freeze-fracture and freeze-drying methodology in conjunction with scanning and transmission electron microscopy (SEM, TEM) and energy-dispersive x-ray spectroscopy (EDS). The secretory- and maturation-stage enamel organ prevented Br from entering the enamel matrix. Br was localized in the Tomes' processes, but not in the enamel matrix, strongly suggesting that the distal intercellular junctions of ameloblasts are "tight". Furosemide disrupted anion transport to allow not only Cl but also Br to enter the forming enamel matrix. Periodic administration of high F doses promoted the formation of bands of disrupted enamel, reflecting the periodicity of F administration. The same concentration of F administered with furosemide increased the severity of disrupted enamel, resulting in "blisters" and pits in the maturing enamel. The enamel "blisters" contained pools of small, disorganized enamel crystallites. The group receiving furosemide only displayed normal enamel structure but had increased Cl in the enamel matrix. This study provides evidence that anion transporters, possibly the Na-K-2Cl co-transporter, function to regulate anion translocation, including F, to the enamel matrix in secretory- and maturation-stage enamel organ. These mechanisms may explain why the ionic composition on the cellular side of the anion barrier is different from that of the enamel matrix.

Ameloblasts↗
PubMed2000

Synergistic effects of iontophoresis and jet injector pretreatment on the in-vitro skin permeation of diclofenac and angiotensin II.

A non-needle syringe (jet injector) was utilized to increase skin permeation of drugs by iontophoresis. Briefly, physiological saline was initially flushed by the injector to make a pore in the stratum corneum of excised hairless rat skin, and the iontophoretic skin permeation of two model compounds, sodium diclofenac and angiotensin II, was followed using a 2-chamber diffusion cell. Constant voltage and constant current iontophoresis treatments were evaluated. Pretreatment using the jet injector alone resulted in about 13- and 22-fold increases in the steady-state flux of diclofenac and angiotensin II, respectively, through the skin, compared with non-treated controls. Jet injector pretreatment with constant voltage iontophoresis further enhanced skin permeation of diclofenac and angiotensin II, and the enhancement was also greater than that by constant voltage iontophoresis alone. Thus, a synergistic effect was observed. The ratio of enhancement was greater compared with the control. Jet injector pretreatment with constant current iontophoresis, however, did not always yield higher skin permeation of the drugs than injector pretreatment alone, although the lag time was shortened. The difference in the enhancement between the constant voltage- and constant current iontophoresis can be explained by the electric current through the excised skin. Constant current iontophoresis after a short period of constant voltage iontophoresis with multiple jet injector pretreatments may be the best way to increase drug permeability while preventing severe skin damage.

Administration, Cutaneous↗