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  • 1
    Electronic Resource
    Electronic Resource
    SYNTHESIS AND RELEASE OF PROSTAGLANDINS BY RAT BRAIN SYNAPTOSOMAL FRACTIONS (1976)
    Oxford, UK : Blackwell Publishing Ltd
    Journal of neurochemistry 26 (1976), S. 0 
    Details
    ISSN: 1471-4159
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Medicine
    Notes: Abstract— Particulate fractions from rat brain homogenate containing the synaptosomes synthesize and release prostaglandins F and E on aerobic incubation. The prostaglandin of the F-typc released could be further identified as proslaglandin F2α using specific radioimmunoassays for prostaglandins F1α, and F2α-. The metabolite 13,14-dihydro-15-keto-prostaglandin F2α could not be detected. The amount of prostaglandins released is dependent on incubation time and temperature as well as pH and osmolarity of the incubation medium. Total brain homogenate released more prostaglandins than purified synaptosomes per mg protein, indicating that synaptosomes are probably not a main source of prostaglandins when compared with other subcellular brain fractions. While prostaglandin synthesis was only moderately increased by the addition of the precursor fatty acid arachidonic acid, anti-inflammatory drugs like indomethacin, high concentrations of some local anaesthetics and Δ1-tetrahydrocannabinol inhibited prostaglandin release. The neurotransmitters noradrenaline, dopamine and 5-hydroxytryptamine did not influence prostaglandin release from the synaptosomal rat brain fractions.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1471-4159.1976.tb01501.x
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  • 2
    Electronic Resource
    Electronic Resource
    Role of Peptidergic Sensory Neurons in Gastric Mucosal Blood Flow and Protection (1991)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 632 (1991), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Notes: The present findings have revealed a new aspect of how mechanisms of gastric mucosal resistance to injury are called into effect and are coordinated by the nervous system. Capsaicin-sensitive sensory neurons in the stomach play a physiological role in monitoring acid influx into the superficial mucosa. Once activated, they strengthen gastric mucosal defense against deep injury, with a key process in this respect being an increase in blood flow through the gastric mucosa. This concept opens up completely new perspectives in the physiology and pathophysiology of the gastric mucosa if we consider that the long-term integrity of the gastric mucosa may be under the subtle control of acid-sensitive sensory neurons and that, vice versa, improper functioning of these neural control mechanisms may predispose to gastric ulcer disease.The present observations also indicate that some of the peptides contained in gastric sensory nerve endings might fulfill a transmitter or mediator role in controlling gastric mucosal blood flow and integrity. Whereas substance P and neurokinin A are unlikely to play a role in the regulation of gastric mucosal blood flow, there is severalfold evidence that CGRP is very important in this respect. This peptide, which in the rat gastric mucosa originates exclusively from spinal sensory neurons,2,4,27 is released upon stimulation of sensory nerve endings and is extremely potent in facilitating gastric mucosal blood flow and in protecting the mucosa from injurious factors. Selective ablation of spinal sensory neurons containing CGRP weakens the resistance of the gastric mucosa against acid injury, which is most likely due to inhibition of protective vasodilator reflexes. We now aim at providing direct pharmacological evidence that antagonism of endogenously released CGRP results in similar pathophysiological consequences as ablation of capsaicin-sensitive sensory neurons.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1991.tb33115.x
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  • 3
    Electronic Resource
    Electronic Resource
    Selectin-P (PADGEM, GMP-140)- mediated Adhesion of Human Platelets to Neutrophils in Vitro and Immune Complex-induced Peritonitis in Rats Is Influenced by Interleukin-8 (1995)
    Oxford, UK : Blackwell Publishing Ltd
    Annals of the New York Academy of Sciences 762 (1995), S. 0 
    Details
    ISSN: 1749-6632
    Source: Blackwell Publishing Journal Backfiles 1879-2005
    Topics: Natural Sciences in General
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1111/j.1749-6632.1995.tb32345.x
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  • 4
    Electronic Resource
    Electronic Resource
    Release of calcitonin gene-related peptide in cardiac anaphylaxis (1997)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 355 (1997), S. 224-229 
    Details
    ISSN: 1432-1912
    Keywords: Key words Cardiac anaphylaxis ; Isolated perfused guinea-pig heart ; Eicosanoids ; Histamine ; Calcitonin gene-related peptide
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We have investigated the antigen-stimulated release of calcitonin gene-related peptide (CGRP) from ovalbumin-sensitized guinea-pig isolated hearts and the interaction with other mediators of anaphylaxis released concomitantly. It was found that antigen challenge caused a significant increase of CGRP release (from basal 31.2 ± 2.9 to 51.6 ± 4.9 fmol/5 min). Anaphylactic CGRP release was significantly attenuated in the presence of the cyclooxygenase inhibitor indomethacin while the 5-lipoxygenase inhibitor Bay-X1005 ((R)-2-[4-quinolin-2-yl-methoxy)phenyl]-2-cyclopentyl acetic acid) had no significant effect. Combined treatment with the histamine receptor (H1,H2) antagonists mepyramine and cimetidine also significantly attenuated anaphylactic release of CGRP. Under control conditions antigen injection increased release of cysteinyl-leukotrienes (LT), thromboxane (TXB2) and 6-keto-prostaglandin (PG)F1α from basal values of 0.96 ± 0.09, 2.7 ± 0.7 and 3.4 ± 0.28 ng/5 min respectively, to 5.9 ± 0.9, 48.4 ± 3.4 and 6.9 ± 1.4 ng/5 min. Indomethacin abolished the release of cyclooxygenase products of arachidonate metabolism and simultaneously increased cysteinyl-LT release significantly (8.8 ± 1.4 ng/5 min). Conversely Bay-X1005 completely abolished cysteinyl-LT release and had no significant effect on anaphylactic release of TXB2 and 6-keto-PGF1α. Simultaneous blockade of H1 and H2 receptors abolished release of 6-keto-PGF1α, while release of TXB2 and cysteinyl-LT was not significantly affected. The results indicate that CGRP is not a primary mediator of the immediate hypersensitivity reaction of the heart, but is in turn released by arachidonic acid metabolites of the cyclooxygenase pathway and histamine. In contrast, LT obviously do not contribute to anaphylactic CGRP release. CGRP is a potent coronary vasodilator and could act as endogenous functional antagonist of vasoconstrictor mediators also released during cardiac anaphylaxis such as cysteinyl-LT, platelet activating factor and TXA2.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/PL00004936
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  • 5
    Electronic Resource
    Electronic Resource
    Prostaglandin, slow-reacting substance, and histamine release from anaphylactic guinea-pig hearts, and its pharmacological modification (1975)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 289 (1975), S. 65-76 
    Details
    ISSN: 1432-1912
    Keywords: Prostaglandins ; Slow-Reacting Substance of Anaphylaxis ; Histamine ; Cardiac Anaphylaxis ; Isoproterenol
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Prostaglandins (Pgs), slow-reacting substance of anaphylaxis (SRS-A), and histamine were released from anaphylactic isolated perfused guinea pig hearts. Pgs were to the greatest part of the F2α-type. PgE2 was found in traces only. Neither PgA2, nor the metabolites 13,14-dihydro-15-keto-PgF2α and 13,14-dihydro-15-keto-PgE2 were detected in the perfusates. Isoproterenol reduced the PgF2α output significantly. This effect was increased by the addition of theophylline. Propranolol did not reverse the effect of isoproterenol, but in a high concentration (5 μg/ml) reduced the PgF2α output for its own. Indomethacin completely abolished the anaphylactic prostaglandin release. The histamine liberation was significantly decreased only by the combination of isoproterenol and theophylline, and also by a high concentration of propranolol (5 μg/ml). In contrast to the Pg release, the anaphylactic SRS-A and histamine liberation was not abolished by indomethacin, but rather increased. The results are discussed in view of the possible role of the released substances in the functional events of cardiac anaphylaxis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498030
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  • 6
    Electronic Resource
    Electronic Resource
    Release of 15-keto-13, 14-dihydro-thromboxane B2 and prostaglandin D2 during anaphylaxis as measured by radioimmunoassay (1978)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 305 (1978), S. 247-252 
    Details
    ISSN: 1432-1912
    Keywords: 15-Keto-13, 14-Dihydro-Thromboxane B2-Thromboxane ; B2-Prostaglandin ; D2-Radioimmunoassay-Anaphylaxis
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. A specific radioimmunoassy for 15-keto-13, 14-dihydro-thromboxane B2 was developed employing a polyvalent 125I-labelled tracer. 2. Using the radioimmunoassay large amounts of immunoreactive 15-keto-13, 14-dihydro-thromboxane B2 were found in perfusates of anaphylactic guinea pig lungs, but not in perfusates of anaphylactic guinea pig hearts. On the other hand, both lungs and hearts released immunoreactive thromboxane B2 after challenge, lungs being, however, much more active. 3. Using a radioimmunoassay for prostaglandin D2 variable amounts of this compound were detected in perfusates of anaphylactic guinea pig lungs. 4. While the cyclo-oxygenase inhibitor indomethacin (1 μg/ml) abolished release of thromboxane B2, 15-keto-13, 14-dihydro-thromboxane B2 and prostaglandins from anaphylactic guinea pig lungs, the thromboxane synthetase inhibitor imidazole (100 μg/ml) was without significant effect. 5. The results indicate that in anaphylactic guinea pig lungs, contrary to anaphylactic guinea pig hearts, a major fraction of the total thromboxane released into the perfusates is in the form of the biologically inactive 15-keto-13, 14-dihydro-thromboxane B2. On the other hand, prostaglandin D2, which can be formed enzymatically or non-enzymatically from the prostaglandin endoperoxide PGH2, might contribute to vascular and bronchial smooth muscle contraction observed in anaphylaxis.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00498818
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  • 7
    Electronic Resource
    Electronic Resource
    Effect of muscarinic receptor stimulation on release of cysteinyl-leukotrienes and thromboxane B2 from anaphylactic guinea-pig hearts (1988)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 338 (1988), S. 577-581 
    Details
    ISSN: 1432-1912
    Keywords: Anaphylaxis ; Guinea-pig heart ; Methacholine ; Cysteinyl-leukotrienes ; Thromboxane B2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of muscarinic receptor stimulation by infusions of methacholine (6.25 × 10−8 mol/min or 1.9 × 10−7 mol/min) into isolated perfused, spontaneously beating sensitized guinea-pig hearts on the anaphylactic release of cysteinyl-leukotrienes (LT) and thromboxane (TX) B2 were investigated. Methacholine increased coronary flow and decreased heart rate under basal conditions. Furthermore, infusions of methacholine (1.9 × 10−7 mol/min) significantly increased the anaphylactic release of TXB2 as well as of immunoreactive cysteinyl-LT, which were demonstrated by reversed phase high pressure liquid chromatography to consist of a mixture of LTC4, LTD4 and LTE4. Infusions of atropine (1.3 × 10−7 mol/min) alone did not significantly affect coronary flow and heart rate prior to ovalbumin injection nor anaphylactic release of cysteinyl-LT. The anaphylactic release of TXB2 was, however, significantly decreased in the presence of atropine. Atropine (1.3 × 10−7 mol/min) infused in addition to methacholine (1.9 × 10−7 mol/min) abolished the effects of the muscarinic receptor agonist on spontaneous heart rate and significantly antagonized the increase in coronary flow prior to ovalbumin injection. Similarly, the simultaneous infusion of atropine abolished the effects of methacholine on the anaphylactic release of TXB2 and cysteinyl-LT. After antigen challenge hearts infused with methacholine, atropine or the combination of both drugs did not exhibit any differences with respect to anaphylactic changes of heart rate or the time course of anaphylactic coronary flow reduction. Thus, in the isolated perfused anaphylactic guinea-pig heart, muscarinic receptor stimulation significantly enhanced the release of the arachidonic acid-derived mediators TXB2 and cysteinyl-LT. This enhanced release of vasoconstrictor eicosanoids was, however, not accompanied by an increased coronary vasoconstriction, probably because of the counter-acting vasodilator effect of methacholine.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00179333
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  • 8
    Electronic Resource
    Electronic Resource
    Modulation of the contractile activity of the guinea-pig lung parenchymal strip by exogenous 5,8,11,14,17-eicosapentaenoic acid (1987)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 335 (1987), S. 652-659 
    Details
    ISSN: 1432-1912
    Keywords: Anaphylaxis ; Eicosapentaenoic acid ; Lung parenchymal strips ; Leukotriene ; Prostaglandin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Exogenous eicosapentaenoic acid (EPA, 16.5 μmol/l or 33 μmol/l) inhibited dose-dependently the anaphylactic contractile response of guinea-pig lung parenchymal strips suspended in an organ bath. As determined by radioimmunoassay, EPA inhibited in a dose-dependent manner the anaphylactic release of the cyclooxygenase products thromboxane (TX) B2 and 6-keto-prostaglandin (PG) F1α but simultaneously enhanced the release of sulfidopeptide (SP)-leukotrienes (LT). Indomethacin (2.8 μmol/1) abolished the release of cyclooxygenase products but potentiated the release of SP-LT. However, indomethacin treatment did not affect the inhibitory action of EPA on the contractile response of the anaphylactic lung strips. The lipoxygenase inhibitor, esculetin (50 μmol/1), inhibited the release of SP-LT and also that of cyclooxygenase products of polyunsaturated fatty acid metabolism. The combination of esculetin and EPA resulted in enhanced inhibition of the anaphylactic contractile response as compared to EPA alone. By reversed phase high pressure liquid chromatography (HPLC), SP-LT from anaphylactic lung parenchymal strips was shown to consist of LTD4 and LTE4. EPA-pretreated lung strips released upon immunologic challenge additional immunoreactivity comigrating with authentic LTC4, LTC5, LTD5 and LTE5. While anaphylactic control strips also released LTB4, in the bath fluid of EPA-treated strips, an additional immunoreactive compound migrating with the retention time of LTB5 was observed. In non-sensitized guinea-pig lung parenchymal strips EPA inhibited the myotropic activity of exogenous mediators such as histamine (9 gmol/1), LTC4 (16 nmol/1) and the TX mimetic U 46619 (28.4 nmol/1), an effect which was neither affected by indomethacin (2.8 gmol/1) nor by the lipoxygenase inhibitor nordihydroguaiaretic acid (NDGA, 10 gmol/1). We conclude that exogenous EPA is able to inhibit the myotropic activity of endogenous and exogenous mediators of the anaphylactic reaction in the guinea-pig lung parenchymal strip. Thus, EPA itself and not a metabolite of the cyclooxygenase or lipoxygenase pathway of polyunsaturated fatty acid metabolism seems to act as a functional antagonist to various anaphylactic mediators in lung tissue.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00166982
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  • 9
    Electronic Resource
    Electronic Resource
    On the relation between release of prostaglandins and contractility of rabbit splenic capsular strips (1976)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 292 (1976), S. 35-42 
    Details
    ISSN: 1432-1912
    Keywords: Prostaglandins ; α-Receptor agonists ; Smooth muscle contraction ; Indometacin ; 5,8,11,14-Eicosatetraynoic acid
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Rabbit splenic capsular strips release prostaglandins E and F when contracted by noradrenaline or methoxamine. Contractions and prostaglandin release are dose-dependent. Cocaine increases significantly the effect of noradrenaline, but not that of methoxamine, on contraction of the strips and release of prostaglandin E. Release of prostaglandin F was increased by the addition of cocaine not only when noradrenaline was used as an agonist but also at two of three dose levels of methoxamine. When indometacin is added to the bath fluid, it inhibits prostaglandin release and at the same time potentiates the contractile effects of noradrenaline and methoxamine on the rabbit splenic capsular strips. The prostaglandin-synthetase blocker 5,8,11,14-eicosatetraynoic acid also potentiates the contractions induced by noradrenaline and methoxamine. Both the effects on prostaglandin synthesis and on contraction exerted by indometacin can be reversed, when indometacin is washed out. Exogenous prostaglandins E1, E2 and F2α in concentrations up to 150 ng/ml do not influence contractions of the strips induced by either noradrenaline or methoxamine. At higher concentrations prostaglandin E1 decreases, but prostaglandins E2 and F2α increase the contractions induced by both agonists. The potentiation of the effects of noradrenaline and methoxamine on rabbit splenic strips by indometacin and 5,8,11,14-eicosatetraynoic acid cannot be explained by inhibition of uptake1 or uptake2, release of endogenous noradrenaline or inhibition of metabolism of the agonists. It is suggested that the potentiation is caused by inhibition of synthesis of endogenous prostaglandins, although an undefined sensitizing effect of indometacin and 5,8,11,14-eicosatetraynoic acid cannot be completely excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00506487
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  • 10
    Electronic Resource
    Electronic Resource
    Influence of prostaglandins on connective tissue cell growth and function (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 297 (1977), S. S89 
    Details
    ISSN: 1432-1912
    Keywords: Prostaglandins ; cAMP ; glycosaminoglycan synthesis ; proliferation ; glucocorticoids ; fibroblasts
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Prostaglandins (PGs) are synthesized by cultured fibroblasts. PGs regulate specific cellular functions by influencing cyclic nucleotide levels. PGE1 increases cAMP levels, thus enhancing glycosaminoglycan (GAG) synthesis and reducing proliferation. Exogenous cyclic nucleotides, on the other hand, affect PG formation. Glucocorticoids (GCs) decrease cAMP content, GAG synthesis and PG formation in fibroblasts, the latter effect occurring only after prolonged incubations. The decrease in endogenous PG levels causes a sensitization of the cells to exogenous PGE1, thus counteracting the initial inhibitory effect of GCs on cAMP content and GAG synthesis. Cell proliferation shows an inverse relationship to PG-induced changes in cAMP levels.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00587790
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