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  • 1
    Electronic Resource
    Electronic Resource
    Contribution of neutrophils to lipopolysaccharide-induced tumor necrosis factor production and mortality in a carrageenan-pretreated mouse model (1997)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 17 (1997), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Carrageenan (CAR) pretreatment primes mice for lipopolysaccharide (LPS)-induced tumor necrosis factor (TNF)-α production in sera and increases their mortality rate. To study the contribution of neutrophils in this model, blood neutrophil count was regulated with cyclophosphamide. After LPS challenge, both serum TNF-α activity and mortality risk ratio were significantly higher in neutrophilic mice, but significantly lower in neutropenic mice. In vitro, CAR treatment primed for TNF-α production of blood neutrophils, but conversely, that of monocytes was suppressed. We suggest that neutrophils are the major cells to produce TNF-α and to determine mouse mortality after LPS challenge in the mouse CAR model.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1997.tb01010.x
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  • 2
    Electronic Resource
    Electronic Resource
    Dextran sulphate enhancement of lipopolysaccharide-induced tumour necrosis factor-α production by murine peritoneal macrophages: Correlation with macrophage blockade (1993)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS immunology and medical microbiology 7 (1993), S. 0 
    Details
    ISSN: 1574-695X
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology , Medicine
    Notes: Abstract Proteose peptone-induced murine peritoneal macrophages (Mø) were preincubated with 100–800 μg/ml of dextran sulphate (DS) 500 (Mr 500 000) or DS1000 (Mr 1 000 000). After 2–24 h of the preincubation, the Mø were stimulated with 1 μg/ml of lipopolysaccharide (LPS) in vitro for 18 h in DS-free culture medium. The culture supernatants were then collected for TNF assay. The LPS-induced TNF activity of Mø supernatant preincubated with DS500 or DS1000 for 6 h was enhanced by up to about ten-fold compared with those preincubated without DS. This enhancing effect was not observed when Mø were preincubated with 100–800 μg/ml of low molecular weight DS5 (Mr 5000) or neutral dextran (Dex) 500 (Mr 500 000). The enhancement of LPS-induced TNF-α production from Mø was observed after 2 or 4 h of incubation with DS1000 or DS500, respectively. The phagocytic activity of Mø was determined in vitro by the ingestion index and phagocytic capacity using Saccharomyces cerevisiae. Treatment with DS500 or DS1000 significantly suppressed the phagocytic activity from 2 h after the incubation, but this suppression was not observed in Mø incubated with DS5 or Dex500. Our experiments indicate that DS500 and DS1000 act directly on Mø and enhance LPS-induced TNF-α production from Mø, and that the enhancement is closely related to the suppression of Mø phagocytic function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-695X.1993.tb00394.x
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  • 3
    Electronic Resource
    Electronic Resource
    Priming effect of dextran sulphates on lipopolysaccharide-induced tumour necrosis factor production in mice (1992)
    Oxford, UK : Blackwell Publishing Ltd
    FEMS microbiology letters 89 (1992), S. 0 
    Details
    ISSN: 1574-6968
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Biology
    Notes: Abstract Dextran sulphate (DS) 500 (M.W. 500 000) is commonly used as a reticuloendothelial (RE) blocker. We found that lipopolysaccharide (LPS)-induced tumour necrosis factor (TNF) production in sera was enhanced when mice were pretreated with DS500. When mice were pretreated with DS1000 (M.W. 1 000 000), TNF activity in sera was also significantly enhanced by the LPS injection in comparison with the saline-treated group, but not by the pretreatment with the low molecular weight of DS5 (M.W. 5 000), neutral dextran (Dex) 500, or positively-charged diethylaminoethyl dextran (DEAE-Dex) 500. The enhancement of LPS-induced TNF production occurred from 2 h after DS500 pretreatment. Pretreatment with DS500 or DS1000 significantly suppressed the carbon clearance from the blood in mice from 2 h after DS injection, but this suppression was not detected by the pretreatment with DS5, Dex500, or DEAE-Dex500. We suggest that negative-charge and high molecular weight are essential for dextran derivatives to enhance LPS-induced TNF production, and that the enhancing effect of DS is closely related to the suppression of the RE function.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1574-6968.1992.tb04984.x
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  • 4
    Electronic Resource
    Electronic Resource
    Isoflurane inhibits nicotinic acetylcholine receptor-mediated 22Na+ influx and muscarinic receptor-evoked cyclic GMP production in cultured bovine adrenal medullary cells (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 349 (1994), S. 223-229 
    Details
    ISSN: 1432-1912
    Keywords: Adrenal medullary cells ; Cyclic GMP ; Isoflurane ; Muscarinic receptor ; Nicotinic receptorion channel complex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of isoflurane on 22Na+ influx, 45Ca2+ influx, catecholamine secretion and cyclic GMP production induced by three kinds of secretagogue (nicotinic agonists, veratridine and a high concentration of K+) have been investigated using cultured bovine adrenal medullary cells. (1) Isoflurane (1–6%) inhibited catecholamine secretion stimulated by carbachol, nicotine and dimethyl-4-phenylpiperazinium in a concentration-dependent manner. Isoflurane suppressed carbachol-evoked 22Na+ influx and 45Ca2+ influx at concentrations similar to those which suppressed catecholamine secretion. The inhibition of catecholamine secretion by isoflurane was not overcome by increasing the concentration of carbachol. (2) The inhibitory effects of isoflurane on veratridine-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion became evident when the concentration of isoflurane was raised to 4–6%, i.e. 2–3 fold higher than the concentrations (1–2%) employed clinically. (3) High K+-evoked 45Ca2+ influx and catecholamine secretion were not affected by isoflurane (1–6%). (4) Isoflurane (1–6%) attenuated the production of cyclic GMP caused by muscarine, but not that caused by atrial natriuretic peptide or by sodium nitroprusside. These results suggest that isoflurane, at clinical anesthetic concentrations, inhibits nicotinic acetylcholine receptor-mediated cell responses as well as muscarinic receptor-mediated cyclic GMP production in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169287
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  • 5
    Electronic Resource
    Electronic Resource
    Inhibitory effects of propofol on catecholamine secretion and uptake in cultured bovine adrenal medullary cells (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 572-578 
    Details
    ISSN: 1432-1912
    Keywords: Adrenal medulla ; Catecholamine secretion ; Inhibition ; 22Na+ influx ; Noradrenaline uptake ; Propofol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the central and peripheral noradrenergic neurons, the balance between noradrenaline release and reuptake determines the level of noradrenaline at the synaptic cleft or the nerve ending. In the present study, we examined the effects of propofol, an intravenous general anaesthetic, on catecholamine secretion and noradrenaline uptake in cultured bovine adrenal medullary cells and on the serum noradrenaline and blood pressure in rats. In cultured adrenal medullary cells, propofol (10–50 μmol/l) concentration-dependently inhibited catecholamine secretion stimulated by carbachol. Propofol suppressed carbachol-evoked 22Na+ influx as well as 45Ca2+ influx at concentrations similar to those which suppressed the catecholamine secretion. Propofol (10–50 μmol/l) also inhibited veratridine-evoked 22Na+ influx, 45Ca2+ influx and catecholamine secretion, whereas it had little effect on the 45Ca2+ influx and catecholamine secretion induced by 56 mmol/l K+. Cultured adrenal medullary cells show [3H] noradrenaline uptake which is sensitive to imipramine. Propofol (10–50 μmol/l) significantly inhibited the imipramine-sensitive uptake of [3H] noradrenaline. In rats, intravenous administration of propofol (2.5 mg/kg) lowered serum noradrenaline and arterial blood pressure. From these findings, in spite of inhibiting noradrenaline uptake, propofol at anaesthetic concentrations (10–30 μmol/l) seems to reduce catecholamine secretion by interfering with Na+ influx through voltage-dependent Na+ channels as well as nicotinic acetylcholine receptor-associated ion channels in the adrenal medulla and, probably, in the sympathetic nervous system. This may explain the propofol-induced hypotension during anaesthesia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169178
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  • 6
    Electronic Resource
    Electronic Resource
    Isoflurane inhibits nicotinic acetylcholine receptor-mediated 22Na+ influx and muscarinic receptor-evoked cyclic GMP production in cultured bovine adrenal medullary cells (1994)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 349 (1994), S. 223-229 
    Details
    ISSN: 1432-1912
    Keywords: Key words: Adrenal medullary cells – Cyclic GMP – Isoflurane – Muscarinic receptor – Nicotinic receptor-ion channel complex
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. The effects of isoflurane on 22Na+ influx, 45Ca2+ influx, catecholamine secretion and cyclic GMP production induced by three kinds of secretagogue (nicotinic agonists, veratridine and a high concentration of K+) have been investigated using cultured bovine adrenal medullary cells. (1) Isoflurane (1–6%) inhibited catecholamine secretion stimulated by carbachol, nicotine and dimethyl-4-phenylpiperazinium in a concentration-dependent manner. Isoflurane suppressed carbachol-evoked 22Na+ influx and 45Ca2+ influx at concentrations similar to those which suppressed catecholamine secretion. The inhibition of catecholamine secretion by isoflurane was not overcome by increasing the concentration of carbachol. (2) The inhibitory effects of isoflurane on veratridine-induced 22Na+ influx, 45Ca2+ influx and catecholamine secretion became evident when the concentration of isoflurane was raised to 4–6%, i.e. 2–3 fold higher than the concentrations (1–2%) employed clinically. (3) High K+-evoked 45Ca2+ influx and catecholamine secretion were not affected by isoflurane (1–6%). (4) Isoflurane (1–6%) attenuated the production of cyclic GMP caused by muscarine, but not that caused by atrial natriuretic peptide or by sodium nitroprusside.   These results suggest that isoflurane, at clinical anesthetic concentrations, inhibits nicotinic acetylcholine receptor-mediated cell responses as well as muscarinic receptor-mediated cyclic GMP production in adrenal medullary cells.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169287
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  • 7
    Electronic Resource
    Electronic Resource
    Inhibitory effects of propofol on catecholamine secretion and uptake in cultured bovine adrenal medullary cells (1996)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 353 (1996), S. 572-578 
    Details
    ISSN: 1432-1912
    Keywords: Key words Adrenal medulla ; Catecholamine secretion ; Inhibition ; 22Na+ influx ; Noradrenaline uptake ; Propofol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In the central and peripheral noradrenergic neurons, the balance between noradrenaline release and reuptake determines the level of noradrenaline at the synaptic cleft or the nerve ending. In the present study, we examined the effects of propofol, an intravenous general anaesthetic, on catecholamine secretion and noradrenaline uptake in cultured bovine adrenal medullary cells and on the serum noradrenaline and blood pressure in rats. In cultured adrenal medullary cells, propofol (10–50 μmol/l) concentration-dependently inhibited catecholamine secretion stimulated by carbachol. Propofol suppressed carbachol-evoked 22Na+ influx as well as 45Ca2+ influx at concentrations similar to those which suppressed the catecholamine secretion. Propofol (10–50 μmol/l) also inhibited veratridine-evoked 22Na+ influx, 45Ca2+ influx and catecholamine secretion, whereas it had little effect on the 45Ca2+ influx and catecholamine secretion induced by 56 mmol/l K+. Cultured adrenal medullary cells show [3H] noradrenaline uptake which is sensitive to imipramine. Propofol (10–50 μmol/l) significantly inhibited the imipramine-sensitive uptake of [3H] noradrenaline. In rats, intravenous administration of propofol (2.5 mg/kg) lowered serum noradrenaline and arterial blood pressure. From these findings, in spite of inhibiting noradrenaline uptake, propofol at anaesthetic concentrations (10–30 μmol/l) seems to reduce catecholamine secretion by interfering with Na+ influx through voltage-dependent Na+ channels as well as nicotinic acetylcholine receptor-associated ion channels in the adrenal medulla and, probably, in the sympathetic nervous system. This may explain the propofol-induced hypotension during anaesthesia.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00169178
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  • 8
    Electronic Resource
    Electronic Resource
    Ketamine interacts with the noradrenaline transporter at a site partly overlapping the desipramine binding site (1998)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 358 (1998), S. 328-333 
    Details
    ISSN: 1432-1912
    Keywords: Key words Adrenal medullary cells ; [3H]Desipramine binding ; Ketamine ; Noradrenaline transporter ; [3H]Noradrenaline uptake ; Xenopus oocytes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Effects of the intravenous anaesthetic ketamine on the desipramine-sensitive noradrenaline transporter (NAT) were examined in cultured bovine adrenal medullary cells and in transfected Xenopus laevis oocytes expressing the bovine NAT (bNAT). Incubation (1–3 h) of adrenal medullary cells with ketamine (10–300 µM) caused an increase in appearance of catecholamines in culture medium. Ketamine (10–1000 µM) inhibited desipramine-sensitive uptake of [3H] noradrenaline (NA) (IC50=97 µM). Saturation analysis showed that ketamine reduced V max of [3H]NA uptake without changing K m, indicating a non-competitive inhibition. Other inhibitors of NAT, namely cocaine and desipramine, showed a competitive inhibition of [3H]NA uptake while a derivative of ketamine, phencyclidine, showed a mixed type of inhibition. Ketamine (10–1000 µM) also inhibited the specific binding of [3H]desipramine to plasma membranes isolated from bovine adrenal medulla. Scatchard analysis of [3H]desipramine binding revealed that ketamine increased K d without altering B max, indicating a competitive inhibition. In transfected Xenopus oocytes expressing the bNAT, ketamine attenuated [3H]NA uptake with a kinetic characteristic similar to that of cultured adrenal medullary cells. These findings are compatible with the idea that ketamine non-competitively inhibits the transport of NA by interacting with a site which partly overlaps the desipramine binding site on the NAT.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005261
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  • 9
    Electronic Resource
    Electronic Resource
    C-type natriuretic peptide inhibits rat mesangial cell proliferation by a phosphorylation-dependent mechanism (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 357 (1997), S. 70-76 
    Details
    ISSN: 1432-1912
    Keywords: Key words C-type natriuretic peptide ; Protein kinase ; Mesangial cell ; Interleukin-1 ; Interleukin-6 ; Angiotensin II ; Platelet derived growth factor
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We studied the effects of C-type natriuretic peptide (CNP) on rat cultured mesangial cell proliferation. (1) Exposure to CNP (10 nM–1 μM for 72 h) inhibited [3H]thymidine incorporation into mesangial cells in a concentration-dependent manner. Atrial natriuretic peptide (1 nM–1 μM), a peptide related to CNP, also decreased [3H]thymidine incorporation into these cells in a concentration-dependent manner. (2) Both CNP (10 nM-1 μM) and atrial natriuretic peptide (10 nM-1 μM) also decreased mesangial cell number. (3) The cyclic GMP analog, 8-bromo-cyclic GMP (100 μM and 1 mM), mimicked the inhibitory effects of CNP and atrial natriuretic peptide on [3H]thymidine incorporation into mesangial cells, whereas inhibitors of protein kinase C, protein kinase A, and protein kinase G reduced the effect of both natriuretic peptides. Moreover, the phoshpatase inhibitor, calyculin A, increased [3H]thymidine incorporation into mesangial cells. (4) CNP and atrial natriuretic peptide decreased interleukin-1-, interleukin-6-, platelet derived growth factor-, angiotensin II-induced [3H]thymidine incorporation into mesangial cells. These results suggest that CNP exerts inhibitory effects on mesangial cell proliferation and that this effects depend on protein phosphorylation pathways.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00005140
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  • 10
    Electronic Resource
    Electronic Resource
    Clinical Study of glucose metabolism during partial gastrectomy (1987)
    Springer
    Journal of anesthesia 1 (1987), S. 82-87 
    Details
    ISSN: 1438-8359
    Keywords: Blood glucose ; Glucose loading ; Insulin ; Epidural anesthesia ; Upper abdominal surgery
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Plasma glucose, insulin, glucagon, growth hormone (GH) and cyclic-AMP (C-AMP) were measured in 14 patients undergoing partial gastrectomy under 5 g/hr glucose loading. Seven patients received general anesthesia (GOF; Group G) and the other seven, GO + epidural anesthesia (analgesia Th4–L1; Group E). Blood glucose increased in both groups, although it remained consistently lower in Group E than in Group G. Serum IRI and IRI/glucose ratio appeared consistently higher in Group E than in Group G and a significant difference was found between the two groups at the early period of surgery. The changes in plasma glucagon and GH were found independent of those in glucose. Cyclic-AMP was also consistently higher in Group G than in Group E and a significant difference was observed at the end of anesthesia. These results suggest that epidural anesthesia with 5 g/hr glucose loading may facilitate insulin release from the islet and peripheral blood uptake particularly during the early period of surgery while many other factors such as GH, cortisol and vagal stimulation seemed to be involved in the later period of surgery. (Ogata M et al.: Clinical study of glucose metabolism during partial gastrectomy; comparison between epidural and general anesthesia. J Anesth 1: 82–87, 1987)
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s0054070010082
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