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PubMed1992

Subsurface demineralization in dental enamel and other permeable solids during acid dissolution.

Subsurface demineralization of dental enamel during acid dissolution has been reported many times, but its cause remains obscure. At first, the phenomenon was thought to result from the physical structure of enamel. More recent studies have shown that subsurface demineralization occurs in other permeable solids, indicating that there must be more fundamental factors involved in this curious effect. In order for this phenomenon to be investigated, dissolution experiments were carried out by means of real-time scanning microradiography in various systems, including enamel, or aggregates of hydroxyapatite (calcium, strontium, or barium), or hydroxides (calcium or magnesium). These were chosen to discriminate between effects of structure and composition. It was found that it was not possible for the demineralization observed in these systems to be attributed to a common feature. From this, it is concluded that subsurface demineralization in enamel and other mineralized tissues should not be ascribed to a single cause.

Acetates↗
PubMed2006

Lipopolysaccharide-induced proliferation and adhesion of U937 cells to endothelial cells involves barium chloride sensitive hyperpolarization.

The adhesion of monocytes to the endothelium and their proliferation in the subendothelial space play an important role in atherosclerosis. Since the proliferation and migration of cells are influenced by the activity of ion channels, the aim of this study was to examine whether barium chloride (Ba(2+))-sensitive potassium channels (K(iCa)) are involved in lipopolysaccharide (LPS)-induced proliferation of monocytic U937 cells, and in the adhesion of these cells to endothelial cells. The adhesion of LPS-stimulated U937 cells to endothelial cells reached a maximum at a concentration of 5 microg/ml. This effect of LPS was completely abolished in the presence of Ba(2+) (100 micromol/l). In addition, LPS-induced proliferation was significantly reduced by Ba(2+) (control, 100%; LPS 5 microg/ml, 175%; LPS + Ba(2+) 100 micromol/l, 136%; n = 12, P < 0.05). To examine whether K(iCa) are activated by LPS, changes of U937 membrane potential were determined. LPS (5 microg/ml) caused a hyperpolarization of U937 cells indicating a flux of K(+) ions out of the cells. This effect was completely blocked by Ba(2+) (100 micromol/l). In conclusion, we demonstrate that LPS activates K(iCa) in U937 cells, which is responsible for LPS-induced adhesion of these cells to endothelial cells, and to the proliferation of U937 cells.

Barium Compounds↗
PubMed2002

Prolonged retention after aggregation into secretory granules of human R183H-growth hormone (GH), a mutant that causes autosomal dominant GH deficiency type II.

Human R183H-GH causes autosomal dominant GH deficiency type II. Because we show here that the mutant hormone is fully bioactive, we have sought to locate an impairment in its progress through the secretory pathway as assessed by pulse chase experiments. Newly synthesized wild-type and R183H-GH were stable when expressed transiently in AtT20 cells, and both formed equivalent amounts of Lubrol-insoluble aggregates within 40 min after synthesis. There was no evidence for intermolecular disulfide bond formation in aggregates of wild-type hormone or the R183H mutant. Both wild-type and R183H-GH were packaged into secretory granules, assessed by the ability of 1 mM BaCl2 to stimulate release and by immunocytochemistry. The mutant differed from wild-type hormone in its retention in the cells after packaging into secretory granules; 50% more R183H-GH than wild-type aggregates were retained in AtT20 cells 120 min after synthesis, and stimulated release of R183H-GH or a mixture of R183H-GH and wild-type that had been retained in the cell was reduced. The longer retention of R183H-GH aggregates indicates that a single point mutation in a protein contained in secretory granules affects the rate of secretory granule release.

Barium Compounds↗
PubMed1991

The ordered secretion of bioactive peptides: oldest or newest first?

The order of secretion of newly synthesized and older bioactive peptides was investigated using primary rat intermediate pituitary melanotropes, which synthesize, store, and secrete peptides derived from pro-ACTH/endorphin (PAE; also POMC). PAE-derived peptides produced by the cells were biosynthetically labeled by incubating the cells with radioactive amino acids at various times preceding the period during which secretion was examined; secreted and cellular peptides were characterized and quantitated by immunoprecipitation, using affinity-purified antibodies to selected regions of PAE, followed by polyacrylamide gel electrophoretic analysis. Release in the absence of secretagogues (basal or constitutive release) was compared to release in the presence of maximally effective levels of 8-bromo-cAMP and BaCl2 (stimulated or regulated release). Both cell types showed short-lived preferential basal release of newly synthesized and not fully mature peptides (less than 2-3 h old). Conversely, the cells showed preferential stimulated secretion of older peptides. A process of maturation occurred, taking 2-4 h, after which the secretion of newly synthesized and older peptides in response to secretagogues was nearly indistinguishable for the smallest product peptides. The data support a model of gradual processing of peptides from precursors into smaller products and maturation from molecules only available for basal release into peptides available for stimulated secretion as well as for basal release. Basal secretion was found to include mature peptides as well as intermediates and precursor molecules. The data do not support the existence of any preferential regulated secretion of newly synthesized peptides.

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed2000

The effects of potassium channel blockers on progesterone-induced suppression of rat portal vein contractility.

The suppression of contractility of rat portal vein caused by progesterone appears to be due to the potassium (K+) channel opening effect of this hormone. The identity of the specific K+ channels involved has been investigated using a variety of K+ channel blockers. Incubation with 100 nM iberiotoxin antagonised the progesterone-induced inhibition of spontaneous and 20 mM K+-induced phasic activity of the portal vein such that the contractions resembled those of the non-progesterone, non-iberiotoxin control tissues treated with the corresponding solvent vehicles. Incubation with barium chloride (20 and 100 microM), 4-aminopyridine (1 mM), tetraethylammonium chloride (1 mM), glibenclamide (1 microM) or apamin (1 microM) did not, however, have the same antagonistic effect. These results suggest that progesterone's selective suppression of rat portal vein contractility is mediated by the opening of BKCa channels.

4-Aminopyridine↗
PubMed2000

Effects of Ba2+ on F&F 96365-sensitive sustained contraction of rat pulmonary artery.

The effects of Ba2+ on receptor-mediated sustained contraction of rat pulmonary artery and guinea-pig oesophageal muscularis mucosae were studied in-vitro. In rat isolated pulmonary artery, sustained contraction induced by noradrenaline (1 microM) was resistant to nicardipine (1 microM), but this same sustained contraction was completely inhibited by SK&F 96365 (30 microM), a blocker of voltage-dependent L-type Ca2+ channels and receptor-activated Ca2+ influx. The SK&F 96365-sensitive sustained contraction induced by noradrenaline (1 microM) may be due primarily to Ca2+ influx through receptor-activated Ca)+ channels resistant to nicardipine. Cumulatively applied BaCl2 (0.1 - 10 mM) increased the noradrenaline (1 microM)-induced sustained contraction of the pulmonary arterial preparation in the absence of nicardipine, but in the presence of nicardipine (1 microM), BaCl2 (0.1 - 3 mM) did not affect this contraction. A higher concentration of BaCl22 (10 mM), however, weakly inhibited the noradrenaline (1 microM)-induced tone. In addition, BaCl2 (3-10 mM) increased the tone induced by KCl (60 mM), and the BaCl2-elevated KCl tone was markedly inhibited by nicardipine (1 microM) treatment. In the guinea-pig isolated oesophageal muscularis mucosae, sustained contraction induced by acetylcholine (3 microM) was resistant to nicardipine (1 microM) but was returned to its basal level by SK&F 96365 (30-60 microM). The SK&F 96365-sensitive, acetylcholine-induced sustained contraction of the oesophageal muscularis mucosae is also likely to link with receptor-activated Ca2+ channels resistant to nicardipine. In contrast to the rat pulmonary artery, cumulatively applied BaC12 (0.3 - 10 mM) inhibited the acetylcholine (3 microM)-induced sustained contraction of the oesophageal muscularis mucosae in a concentration-dependent manner in the presence of nicardipine (1 microM). In conclusion, Ba2+ presumably activates voltage-dependent Ca2+ channels by depolarizing plasma membrane and also passes through voltage-dependent Ca2+ channels to contract the pulmonary artery in the absence of nicardipine, and Ba2+ also has a minor effect on the nicardipine-resistant, SK&F 96365-sensitive sustained contraction induced by noradrenaline in rat isolated pulmonary artery.

Acetylcholine↗
PubMed2003

Involvement of inwardly rectifying K+ channels in secretory responses of human ileal mucosa.

In acute secretory diarrhoea the primary event driving fluid secretion is a transcellular, electrogenic, serosal to mucosal transport of chloride ions. Such transport requires the maintenance of an electrically negative cell membrane voltage, which is achieved through a basolateral outward leakage of potassium ions. The aim of this study was to investigate the nature of K(+) channel involvement in facilitating secretory processes in the human ileum. Muscle-stripped mucosal preparations of human ileal mucosa were set up in Ussing chambers for recording short-circuit current and transmucosal conductance. Escherichia coli heat-stable toxin and vasoactive intestinal peptide (VIP) produced concentration-dependent increases in short-circuit current. Responses to the heat-stable toxin were unaffected by basolateral application of 4-aminopyridine (5 mM), glibenclamide (10 microM) or a combination of charybdotoxin (0.3 microM) plus apamin (0.3 microM). However, basolateral barium (0.2-5 mM) caused a concentration-dependent inhibition. Responses to VIP were similarly affected by barium (0.05-1 mM). These results suggested that electrogenic chloride transport by human ileal mucosa required the presence of basolateral K(+) channels. The use of selective K(+)-channel inhibitors and low concentrations of barium suggested that the channels involved might be of the inwardly rectifying type.

4-Aminopyridine↗
PubMed2003

The color change in CO2 absorbents on drying: an in vitro study using moisture analysis.

UNLABELLED: Alkali hydroxide-free absorbents change color markedly when they dry, whereas absorbents containing alkali hydroxides do not. We investigated whether this observation can be explained by the weaker hygroscopic properties of pure calcium hydroxide compared with alkali hydroxides. Samples of the alkali hydroxide-free absorbents Amsorb or Superia and samples of these two absorbents with 1% or 3% NaOH or 3% KOH added were dried in a moisture analyzer at 105 degrees C to determine their moisture content and to assess the color of the samples during drying (each group, n = 5). Additionally, we repeated the experiments with pulverized samples of Baralyme and Spherasorb, which contain approximately 4% KOH and 1% NaOH, respectively. Amsorb and Superia changed color long before they were dry. After the addition of 1% NaOH, and as with the Spherasorb samples, the drying time required for a color change was longer, and the intensity of the resulting violet was less. This effect was even stronger when 3% NaOH was added. The samples with added KOH and the Baralyme did not change color at all on drying. We conclude that the differences in color change on drying in absorbents with varying NaOH or KOH content cannot be explained by larger water retention because of the hygroscopic properties of the alkali hydroxides. IMPLICATIONS: In an in vitro study, the moisture content and color change on drying were determined in samples of Amsorb or Superia and in the same absorbents with added NaOH or KOH. With increasing concentrations of alkali hydroxide, a delay in the color change upon drying was observed. However, the moisture content did not change.

Absorption↗
PubMed2004

Fires from the interaction of anesthetics with desiccated absorbent.

Rarely, fire and patient injury have resulted from the degradation of sevoflurane by desiccated carbon dioxide absorbent. Desiccated absorbent also can degrade desflurane and isoflurane, and in the present investigation we sought to determine whether a danger of fire also arose with their use in the presence of desiccated absorbent. Baralyme was desiccated by heating and directing a 10 L/min flow of oxygen through the absorbent. Approximately 1200 g of this desiccated absorbent was used to fill a standard absorber placed in a standard anesthetic circuit to which we directed a 6 L/min flow of oxygen containing 1.5 or 3.0 MAC desflurane, isoflurane, or sevoflurane. A 3-L reservoir bag served as a surrogate lung, and we ventilated this lung with a minute ventilation of 10 L/min. With desflurane or isoflurane, at both 1.5 MAC and 3.0 MAC, temperatures increased in 30 to 70 min to a peak of approximately 100 degrees C and then decreased. With 1.5 MAC sevoflurane (3.0 MAC was not studied), temperatures increased to over 200 degrees C, and in 2 of 5 studies, flames appeared in the anesthetic circuit. In a separate study, we found that concurrent delivery of carbon dioxide and desflurane did not increase peak temperatures. We conclude that the interaction of desflurane or isoflurane with desiccated absorbent is not likely to produce the conflagrations possible with sevoflurane.

Barium Compounds↗
PubMed2005

Barium hydroxide lime turns yellow after desiccation.

Ethyl violet is added to carbon dioxide absorbents and normally serves as an indicator of absorbent exhaustion. During the course of several prior studies of anesthetic breakdown, we noted (but did not publish) that barium hydroxide lime (BL), but not soda lime, turns yellow upon desiccation. We hypothesize that ethyl violet undergoes chemical reaction to produce a yellow colorant in desiccated BL. We qualitatively studied the time course of yellow color development during desiccation of these absorbents with dry oxygen. The yellow colorant was extracted from desiccated absorbent with diethyl ether, separated with chromatography, and analyzed with proton nuclear magnetic resonance and combined gas chromatography and mass spectrometry. The yellow color develops after BL has reached nearly complete desiccation. We successfully identified that ethyl violet decomposes into the yellow colorant 4,4'-bis(diethylamino)benzophenone upon desiccation of BL. The color is not intense, is not useful for identifying low levels of absorbent desiccation, and may be difficult to see through tinted canisters. It may be possible for BL to be sufficiently desiccated to allow chemical breakdown of anesthetics, but not yet show yellow coloration. However, if yellow coloration exists, one should assume that it has become desiccated.

Anesthesiology↗
PubMed2005

Temperatures in soda lime during degradation of desflurane, isoflurane, and sevoflurane by desiccated soda lime.

Rarely, fire and patient injury result from the degradation of sevoflurane by desiccated Baralyme. The present investigation sought to determine whether high temperatures also arose with sevoflurane use in the presence of desiccated soda lime. We desiccated soda lime by directing a 10 L/min flow of oxygen through fresh absorbent. Using 1140 +/- 30 g (mean +/- sd) of this desiccated absorbent, we filled a single standard absorber canister placed in a standard anesthetic circuit to which we directed a 6 L/min flow of oxygen containing 1.5 minimum alveolar concentration (MAC) desflurane or sevoflurane, or 3.0 MAC desflurane, isoflurane, or sevoflurane (with and without concurrent delivery of 200 mL/min carbon dioxide). In an additional test, 2 canisters (rather than a single canister) containing desiccated absorbent were used and 3.0 MAC sevoflurane was applied. A 3-L reservoir bag served as a surrogate lung, and we ventilated this lung with a minute ventilation of 10 L/min. With desflurane at 1.5 MAC or 3.0 MAC or isoflurane at 3.0 MAC temperatures increased in 20 to 40 min to a peak of 30 degrees C to 45 degrees C and then declined. With 1.5 or 3.0 MAC sevoflurane, temperatures increased to approximately 90 degrees C, after which temperatures declined. Concurrent delivery of carbon dioxide and sevoflurane did not increase the peak temperatures reached. The use of 2 canisters increased the duration but not the peak of increased temperature reached with 3.0 MAC sevoflurane. No fires resulted from degradation of any anesthetic.

Anesthetics, Inhalation↗
PubMed2006

Vasodilation mediated by inward rectifier K+ channels in cerebral microvessels of hypertensive and normotensive rats.

Although inward rectifier K+ channels contribute to the regulation of cerebral circulation, dilation of cerebral microvasculature mediated by these channels has not been demonstrated in chronic hypertension. We designed the present study to examine the roles of inward rectifier K+ channels in the vasodilation produced by increased levels of extracellular K+ in cerebral parenchymal arterioles from hypertensive and normotensive rats. During constriction to prostaglandin F2alpha (5 x 10(-7) M), the arterioles within brain slices were evaluated using computer-assisted microscopy. Potassium chloride (KCl) induced vasodilation in cerebral arterioles from normotensive (5-10 mM) and hypertensive (5-15 mM) rats, whereas an inward rectifier K+ channel antagonist barium chloride (BaCl2; 10(-5) M) completely abolished the vasodilation in both strains. In arterioles of hypertensive rats, vasodilator responses to KCl were augmented compared with those in normotensive rats. In contrast, the vasodilator responses induced by sodium nitroprusside (3 x 10(-8) to 3 x 10(-6) M) in these two strains were similar. These results suggest that in cerebral cortex parenchymal microvessels, inward rectifier K+ channels play a crucial role in vasodilation produced by extracellular K+ and that the dilation of cerebral arterioles via these channels is augmented in chronic hypertension.

Animals↗
PubMed1996

Mechanism of endothelial cell shape change and cytoskeletal remodeling in response to fluid shear stress.

Endothelium exposed to fluid shear stress (FSS) undergoes cell shape change, alignment and microfilament network remodeling in the direction of flow by an unknown mechanism. In this study we explore the role of tyrosine kinase (TK) activity, intracellular calcium ([Ca2+]i), mechanosensitive channels and cytoskeleton in the mechanism of cell shape change and actin stress fiber induction in bovine aortic endothelium (BAE). We report that FSS induces beta-actin mRNA in a time- and magnitude-dependent fashion. Treatment with quin2-AM to chelate intracellular calcium release and herbimycin A to inhibit TK activity abolished BAE shape change and actin stress fiber induction by FSS, while inhibition of protein kinase C with chelerythrine had no effect. Altering intermediate filament structure with acrylamide did not affect alignment or F-actin induction by FSS. Examining the role of the BAE cytoskeleton revealed a critical role for microtubules (MT). MT disruption with nocodazole blocked both FSS-induced morphological change and actin stress fiber induction. In contrast, MT hyperpolymerization with taxol attenuated the cell shape change but did not prevent actin stress fiber induction under flow. Mechanosensitive channels were found not to be involved in the FSS-induced shape change. Blocking the shear-activated current (IK.S) with barium and the stretch-activated cation channels (ISA) with gadolinium had no effect on the shear-induced changes in morphology and cytoskeleton. In summary, FSS has a profound effect on endothelial shape and F-actin network by a mechanism which depends on TK activity, intracellular calcium, and an intact microtubule network, but is independent of protein kinase C, intermediate filaments and shear- and stretch-activated mechanosensitive channels.

Acrylamide↗
PubMed2004

The transepithelial voltage of the isolated anterior stomach of mosquito larvae (Aedes aegypti): pharmacological characterization of the serotonin-stimulated cells.

The lumen-negative transepithelial voltage (V(te)) of the isolated and perfused anterior stomach of mosquito larvae (Aedes aegypti) was studied with a 'semi-open' preparation in which one end of the gut was ligated onto a perfusion pipette and the other end remained open to the bath. All experiments were performed with serotonin-stimulated preparations. V(te) was abolished after addition of 2.5 mmol l(-1) dinitrophenol and depended on the presence of Cl(-). Na(+) substitution experiments showed that a major part of V(te) depended on the presence of this cation in the hemolymph side of the epithelium. Addition of 10 micro mol l(-1) concanamycin (78+/-6% inhibition) or 2.5 mmol l(-1) ouabain (15+/-2% inhibition) to the bath partially inhibited V(te). DPC (0.5 mmol l(-1)) or DIDS (0.1 mmol l(-1)) reduced V(te) when applied to the hemolymph side of the epithelium (to 49+/-8% or 78+/-3% of the control, respectively). When present on both sides of the epithelium, these inhibitors caused further V(te) reductions (to 23+/-4% or 35+/-4% of the control, respectively). Hemolymph-side furosemide (0.1 mmol l(-1)) or BaCl(2) (5 mmol l(-1)) reduced V(te) by 13+/-3% or 23+/-4% of the control, respectively. When applied to the hemolymph side of the epithelium, amiloride (0.2 mmol l(-1)) significantly decreased V(te) by 35+/-6% of the control, whereas the drug caused no further effect when it was subsequently also applied to the luminal side of the epithelium. The above results are the basis for an extended model for the cellular mechanisms of NaHCO(3) secretion/HCl absorption involved in alkalization of the anterior stomach of mosquito larvae.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1991

Serotonin depresses the after-hyperpolarization through the inhibition of the Na+/K+ electrogenic pump in T sensory neurones of the leech.

In T sensory neurones of the leech, a train of impulses elicited by intracellular electrical stimulation leads to an after-hyperpolarization of up to 30 mV, mainly due to the activation of the electrogenic Na+/K(+)-ATPase but partly to a Ca2(+)-activated K+ conductance. It was found that serotonin reversibly reduced the amplitude of this after-hyperpolarization. We investigated the mechanism of action of serotonin and found: (1) after inhibition of the Ca2(+)-activated K+ conductance with BaCl2 or CdCl2, serotonin was still able to reduce the after-hyperpolarization; (2) when penetration of T cells with microelectrodes leaking sodium was preceded by serotonin perfusion of the ganglia, the normal hyperpolarization due to the activation of the electrogenic pump was converted to a depolarization; (3) after long-lasting perfusion with K(+)-free saline solution (which inhibits the Na+/K+ pump), the application of CsCl caused repolarization by reactivating the electrogenic ATPase; serotonin slowed and reduced this repolarization; (4) serotonin potentiated the depolarization of T neurones caused by the inhibition of the Na+/K+ pump following cooling of ganglia and depressed the hyperpolarization after rewarming to room temperature. These data taken together suggest that serotonin directly inhibits the Na+/K+ electrogenic pump.

Action Potentials↗
PubMed1991

Roles of potassium and chloride ions in cAMP-mediated amylase exocytosis from rat parotid acini.

The roles of potassium and chloride ions in cAMP-mediated amylase exocytosis were studied using intact and saponin-permeabilized parotid acini. Cyclic AMP-evoked amylase release from saponin-permeabilized parotid acini decreased markedly when KCl in the incubation medium was isoosmotically replaced by K-glutamate, NaCl, Na-isothionate, or mannitol. Quinidine and barium, K+ channel blockers, clearly inhibited amylase release from the permeabilized acini, but not from intact ones. The chloride channel blocker DPC (diphenylamine-2-carboxylate) also inhibited amylase release, while DIDS (4,4'-diisothiocyanostilben-2,2'-disulfonate) or bumetanide had little effect, if any, on the exocytosis. Hyperosmolarity with mannitol markedly reduced amylase release from permeabilized acini. These results suggest that potassium and chloride ions play important roles in cAMP-mediated amylase exocytosis, and that these ions act on secretory granules inside the acinar cells.

Amylases↗
PubMed1996

Pharmacological studies on antidiarrheal effects of Hange-shashin-to.

We attempted to characterize the antidiarrheal action of Hange-shashin-to (TJ-14), a kampo medicine, by comparing its action with that of loperamide. The oral administration of TJ-14 caused the dose-dependent suppression of castor oil-induced diarrhea at 250 to 1000 mg/kg. No significant repression was noted by TJ-14 even at 1000 mg/kg, p.o. for diarrhea induced by pilocarpine, serotonin or barium chloride. Oral treatment with loperamide at 5 mg/kg markedly suppressed diarrhea induced by castor oil and barium chloride. Contractions of isolated guinea pig ileum in response to acetylcholine (1 x 10(-7) g/ml), histamine (1 x 10(-7) g/ml) or barium chloride (3 x 10(-4) g/ml) were little affected by TJ-14 at 10(-4) g/ml. The responses elicited by the three contractive drugs were dose-dependently suppressed by loperamide. TJ-14 did not affect the small intestinal transit even at an oral dose of 1000 mg/kg. On the other hand, the small intestinal transit was significantly suppressed by loperamide (5 mg/kg, p.o.). These results indicate that TJ-14 can effectively control castor oil-induced diarrhea, and that its antidiarrheal action was not based on the suppression of intestinal motility.

Animals↗