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  • 11
    Electronic Resource
    Electronic Resource
    Local release of histamine, prostaglandin F2α and thromboxane B2 into the tracheal lumen and its influence on airways reactivity (1984)
    Springer
    Journal of molecular medicine 62 (1984), S. 315-322 
    Details
    ISSN: 1432-1440
    Keywords: Histamine ; Prostaglandin F2α ; Thromboxane B2 ; Mediator release ; Airways reactivity
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The influence of tracheal lavage with ascaris extract (AE) on airway response to acetylcholine (ACH) and histamine (Hi) was investigated in a series of 24 dogs. AE administered to a restricted area of the trachea resulted in a release of various mediators such as Hi, prostaglandin F2α (PGF2α, measured as the metabolite 15-keto-13, 14-dihydro-PGF2α) and thromboxane B2 (TXB2) into the tracheal lumen. This differed from H2O administration which resulted in no increased release of these mediators. The relatively small concentrations of these substances measured in arterial plasma argue for the role of these mediators on a local basis. On the other hand, tracheal lavage with allergen induced changes in airway response to ACH and Hi aerosols which was not observed after tracheal lavage with water. An interaction between this allergen-induced mediator release into the trachea and peripheral airways reactivity could be demonstrated.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01716448
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  • 12
    Electronic Resource
    Electronic Resource
    Enhanced formation of sulfidopeptide-leukotrienes in ulcerative colitis and Crohn's disease: inhibition by sulfasalazine and 5-aminosalicylic acid (1986)
    Springer
    Inflammation research 18 (1986), S. 381-383 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Release of sulfidopeptide (SP)-leukotrienes (LT)in vitro from normal human colonic mucosa and from mucosal tissue obtained from patients with Crohn's disease (CD) and ulcerative colitis (UC) was investigated. It was found that inflamed mucosal tissue released significantly more SP-LT than normal colonic mucosa both under control conditions and after addition of calcium ionophore A23187. These results indicate the presence of endogenous stimuli as well as an increased responsiveness to an exogenous stimulus of LT formation in the inflamed mucosa. Sulfasalazine (SASP), a drug used in inflammatory bowel diseases, and its active metabolite 5-aminosalicylic acid (5-ASA) were found to inhibit colonic mucosal SP-LT formation, while only 5-ASA inhibited simultaneously synthesis of another arachidonic acid-derived inflammatory mediator, prostaglandin (PG) E2. The results suggest that SP-LT might be important mediators of inflammation in CD and UC.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01965001
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  • 13
    Electronic Resource
    Electronic Resource
    Effect of a new anti-inflammatory compound, CGP 28237, on arachidonate metabolism in rat gastrointestinal tissue (1988)
    Springer
    Inflammation research 23 (1988), S. 110-111 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01967208
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  • 14
    Electronic Resource
    Electronic Resource
    Inhibition of cysteinyl-leukotriene production by azelastine and its biological significance (1988)
    Springer
    Inflammation research 24 (1988), S. 217-223 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Azelastine is a phthalazinone derivative with a wide spectrum of pharmacological activities. Actively sensitized guinea pigs were used to examine the broncholytic effect of azelastinein vivo. Furthermore, the influence of azelastine on the production of arachidonic acid (AA) metabolites was investigatedin vitro and compared to the effects of nordihydroguaiaretic acid (NDGA), indomethacin and ketotifen.In vivo, azelastine protected actively sensitized guinea-pigs against ovalbumin-induced bronchospasm with an ID50 of 0.08 mg/kg orally. Ketotifen was similarly active (ID50=0.05 mg/kg). Antigen-induced contraction of isolated tracheal rings of sensitized guinea-pigs was concentration-dependently inhibited by azelastine and NDGA with IC50-values of 94.1 and 34.2 μmol/l, respectively. Ketotifen exerted only weak inhibitory activity (18% at 100 μmol/l). The arachidonic acid-induced contraction of isolated guinea-pig tracheal rings was also inhibited both by azelastine (IC50=92.6 μmol/l) and NDGA (IC50=20.4 μmol/l). Ketotifen was inactive on this model. Antigen challenge of chopped lung tissue from sensitized guinea-pigs resulted in the release of cysteinyl-leukotrienes (LT) which were identified by reversed phase high pressure liquid chromatography (HPLC) as LTD4 and LTE4. The release of cysteinyl-LT from sensitized guinea-pig lung tissue induced by antigen challenge was concentration-dependently inhibited by azelastine (IC50=35.2 μmol/l) and NDGA (IC50=8.4 μmol/l) but not by ketotifen and indomethacin. By contrast, indomethacin caused a pronounced augmentation of cysteinyl-LT release. The concentration of indomethacin, which augmented cysteinyl-LT release by 50% was 0.19 μmol/l. At the same concentration, indomethacin inhibited the release of 6-keto-PGF1α and TXB2 by about 50%. Azelastine negligible influenced 6-keto-PGF1α and slightly diminished TXB2 release from the chopped lung tissue after challenge. Its IC50-values were 〉2 mmol/l and 443 μmol/l, respectively. NDGA inhibited the release of 6-keto-PGF1α and TXB2 with IC50-values of 47.3 and 38.3 μmol/l, respectively. Ketotifen was ineffective in inhibiting the release of cyclo-oxygenase products of AA metabolism. It seems likely that inhibition of release of 5-lipoxygenase-derived products of AA metabolism by azelastine contributes to its antiallergic and antiasthmatic activity.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02028274
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  • 15
    Electronic Resource
    Electronic Resource
    Release of 15-hydroxy-5,8,11,13-eicosatetraenoic acid and cysteinyl-leukotrienes in carrageenin-induced inflammation: Effect of non-steroidal anti-inflammatory drugs (1991)
    Springer
    Inflammation research 33 (1991), S. 240-246 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Inflammatory exudates obtained in rats after subcutaneous implantation of carrageenin-soaked sponges were found to contain relatively large amounts of 15-hydroxy-5,8,11,13-eicosatetraenoic acid (15-HETE) and smaller amounts of cysteinyl-leukotrienes (LT) in addition to LTB4, thromboxane (TX) B2 and prostaglandin (PG) E2. Concentrations of 15-HETE and cysteinyl-LT were high 5 hours after sponge implantation and decreased significantly within 24 hours. This time-course, which is smilar to that of TXB2, but differs from that of PGE2, suggests migrating leukocytes as a major source of 15-HETE and cysteinyl-LT. Aspirin, sodium salicylate, dipyrone (100 mg/kg each) and indomethacin (2 and 20 mg/kg) decrease the concentrations of cyclooxygenase products of arachidonate metabolism, but did not significantly affect levels of 15-HETE. Cysteinyl-LT were increased by 20 mg/kg indomethacin, but remained unaffected by 2 mg/kg indomethacin and by the other non-steroidal anti-inflammatory drugs (NSAID) tested. 15-HETE and cysteinyl-LT could play a mediator role in inflammation. In addition, they could modulate the release and effects of other inflammatory mediators.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01986569
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  • 16
    Electronic Resource
    Electronic Resource
    Effect of prostaglandin E2 and 3-morpholinosydnonimine (SIN-1) on arachidonic acid metabolism in fMLP-stimulated rat neutrophils and on thrombin-induced human platelet aggregation (1992)
    Springer
    Inflammation research 36 (1992), S. 77-82 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of prostaglandin (PG) E2 and the nitric oxide (NO) donor SIN-1 on leukotriene (LT) release from formyl-methionyl-leucyl-phenylalanine (fMLP) (100 nM)-stimulated rat peritoneal neutrophils (RPN) and on thrombin-induced aggregation of washed human platelets were investigated. Both PGE2 (1–100 nM) and SIN-1 (30–300 μM) inhibited release of LTB4 and cysteinyl-LT from RPN in a concentration-dependent manner. The combined effects of PGE2 and SIN-1 were not greater than expected by summation. On the other hand, the inhibitory effect of SIN-1 (0.5 or 1.0 μM) on platelet aggregation was potentiated by PGE2 (0.3–5 μM) in a concentration-dependent manner, while PGE2 alone in the concentrations used had only marginal effects. The results suggest differential regulation of platelet and leukocyte functions by the mediators PGE2 and NO, which could be relevant for various physiological and pathophysiological conditions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01991232
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  • 17
    Electronic Resource
    Electronic Resource
    Eicosanoid release in the endotoxin-primed isolated perfused rat lung and its pharmacological modification (1999)
    Springer
    Inflammation research 48 (1999), S. 632-636 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Rat lung — Endotoxin — FMLP — Eicosanoids — Cyclooxygenases — 5-Lipoxygenase
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: Recent observations have demonstrated a central role of the "inducible" isoform of the cyclooxygenase (COX), COX-2, in the rat lung. Therefore, the reported capacity of selective COX-2 inhibitors to potentiate the formation of leukotriene (LT) B4 may raise concern about pro-inflammatory side effects of such drugs in the respiratory system. The present study was aimed at determining the effects of the COX-2 inhibitor NS-398 on the release of COX and 5-lipoxygenase (LOX) metabolites of arachidonic acid in isolated perfused lungs obtained from endotoxin-treated rats before and after stimulation with the leukocyte secretagogue N-formyl-methionyl-leucyl-phenylalanine (FMLP).¶Methods: Two hours after rats had received endotoxin i.v., the lung was dissected and perfused via the pulmonary artery with physiological salt solution. After an equilibration period of 20 min the outflow was collected (5-min fractions). In the respective treatment groups, indomethacin, NS-398, or the 5-LOX inhibitor MK886 were present throughout the experiment, while FMLP was added to the perfusate during a single 5-min period. The concentration of eicosanoids in the outflow was determined by radioimmunoassay.¶Results: Endotoxin treatment of rats resulted in in-creased expression of COX-2 mRNA in lung tissue, and an elevated basal release of the prostaglandin (PG)I2 metabolite 6-keto PGF1α, without a detectable increase of leukotriene (LT) formation. In-vitro exposure to FMLP stimulated LT and prostanoid release, which was significantly enhanced in endotoxin-primed lungs, and was suppressed by the 5-LOX inhibitor MK-886 (3 μM) and the COX-inhibitor indomethacin (5 μM), respectively. Either compound showed selective inhibition of the respective pathway of arachidonic acid metabolism. In endotoxin-primed lungs, the COX-2 inhibitor NS-398 (0.3-1.0 μM) depressed basal as well as FMLP-stimulated release of 6-keto PGF1α, but did not cause a significant increase of LTB4 or cysteinyl-LT release.¶Conclusions: These results suggest that FMLP, presumably acting on inflammatory cells trapped in the pulmonary circulation of endotoxin treated rats, induced prostanoid formation mainly via the COX-2 pathway, and that its inhibition by NS-398 had no detectable potentiating effect on LTB4 or cysteinyl-LT biosynthesis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050514
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  • 18
    Electronic Resource
    Electronic Resource
    Effect of 5-aminosalicylic acid and 4-aminosalicylic acid on precontracted rat aortic strips and on NO-mediated inhibition of platelet aggregation (1994)
    Springer
    Inflammation research 41 (1994), S. C235 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have examined the interactions of 5-aminosalicylic acid (5-ASA) and 4-aminosalicylic acid (4-ASA) with nitric oxide (NO) on rat aorta and human platelets. Phennylephrine-precontracted rat aortic strips with intact endothelium were further contracted by 5-ASA (50–200 μmol/1) and 4-ASA (1–20 mmol/1) in a concentration-dependent manner. Removal of endothelium, inhibition of guanylate cyclase by methylene blue, inhibition of NO biosynthesis byN G-nitro-l-arginine as well as inactivation of NO by oxyhemoglobin abolished the effects of 5-ASA and 4-ASA. The antiaggregatory effects of 3-morpholinosydnonimine (SIN-1) and rat peritoneal neutrophils (RPN) were diminished in a concentration-dependent manner by 5-ASA (50–250 μmol/l), but not by 4-ASA (up to 20 mmol/l). In the presence of superoxide dismutase (SOD), 5-ASA did not antagonize NO-mediated effects on platelets. 5-ASA up to 100 μmol/l did not affect NO synthase from rat brain, while a concentration of 1 mM caused 21% inhibition. Since NO might act as a cytotoxic mediator, our results suggest that inactivation of NO by 5-ASA and higher concentrations of 4-ASA could contribute to the therapeutic activity of the drugs in inflammatory bowel disease (IBD).
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01987651
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  • 19
    Electronic Resource
    Electronic Resource
    Effect of histamine, acetylcholine and compound 48/80 on bronchoconstriction and release of eicosanoids in the dog (1984)
    Springer
    Inflammation research 15 (1984), S. 153-161 
    Details
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract The effects of Hi and ACH aerosol and of intravenous infusion of compound 48/80 on bronchoconstriction and plasma levels of Hi, TXB2, KH2PGF2α and KH2PGE2 were investigated in 11 bastard dogs. Administration of Hi and ACH aerosol induced bronchoconstriction accompanied by an increase in the plasma levels of Hi and TXB2. No effect on the plasma levels of KH2PGF2α and KH2PGE2 was detected. Release of endogenous Hi by compound 48/80 induced bronchoconstriction and significant increases in the plasma levels of TXB2 as well as of KH2PGF2α and KH2PGE2. The effects of a second administration of Hi and ACH aerosols after compound 48/80 did not differ qualitatively from the effects of the first aerosol administration. However, quantitatively, the second Hi aerosol induced significantly less bronchoconstriction and TXB2 release. Similarly, effects of the second ACH aerosol tended to be decreased as compared to the first ACH aerosol, although the difference was not significant. The diminished effect of the agonists could be due to receptor desensibilization and/or release of adrenaline, which in turn decreases bronchoconstriction and eicosanoid release.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01972342
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  • 20
    Electronic Resource
    Electronic Resource
    Effects of the cyclooxygenase-2 inhibitor NS-398 on thromboxane and leukotriene synthesis in rat peritoneal cells (1998)
    Springer
    Inflammation research 47 (1998), S. 227-230 
    Details
    ISSN: 1420-908X
    Keywords: Key words: Cyclooxygenase — Peritoneal cells — Eicosanoids — Leukotrienes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract. Objective: Inhibition of inducible cyclooxygenase (COX)-2 has been suggested to offer therapeutic advantages without some side effects associated with the inhibition of constitutive COX activity. These side effects encompass asthmatic responses that can be induced by analgesic/antiphlogistic drugs and are possibly related to increased leukotriene (LT) biosynthesis. We have therefore investigated whether or not the selective COX-2 inhibitor NS-398, similar to indomethacin, stimulates leukotriene (LT) biosynthesis in rat peritoneal cells.¶Methods: Three hours after rats had received intraperitoneal injections of bacterial lipopolysaccharide (LPS) or saline, cells were obtained by peritoneal lavage. Northern blot analysis confirmed induction of COX-2 mRNA by LPS treatment. For determination of eicosanoid biosynthesis, peritoneal cells were incubated in the presence of various concentrations of test compounds for 60 min. The supernatants were used for radioimmunological determination of immunoreactive eicosanoids.¶Results: In cells from LPS treated rats, but not in controls, NS-398 (10–300 nM) reduced the amount of TXB2-like immunoreactivity (IR) in the supernatants, the maximum effect being a 25% inhibition. At these concentrations, there was no detectable effect of NS-398 on the amount of LTB4-IR or LTC4-IR in the supernatants. At higher concentrations (1–10 μM), NS-398 caused further inhibition of TXB2 synthesis, an effect that was observed also in non-LPS treated preparations. A significant increase of LTB4-IR was caused by 3–10 μM NS-398. Indomethacin (3–100 nM) reduced the amount of TXB2-IR, and at 〉10 nM increased the amount of LTB4- and LTC4-IR in the supernatant.¶Conclusions: The results show that concentrations of NS-398 that selectively inhibited COX-2 activity, produced no detectable increase in LT biosynthesis, thus raising the possibility that COX-2 inhibitors are less likely than non-selective COX inhibitors to produce LT-related side effects.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s000110050321
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