Library

X
feed icon rss

Your email was sent successfully. Check your inbox.

An error occurred while sending the email. Please try again.

Proceed reservation?

Export
  • 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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 2
    Electronic Resource
    Electronic Resource
    Pharmacological control of prostaglandin and thromboxane release from macrophages (1978)
    [s.l.] : Nature Publishing Group
    Nature 274 (1978), S. 261-263 
    Details
    ISSN: 1476-4687
    Source: Nature Archives 1869 - 2009
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Notes: [Auszug] Table 1 shows that phagocytosis of antibody-coated ery-throcytes (EA) triggered release of mainly immunoactive PGE2 but also of measurable amounts of thromboxane B2 (TXB2) (and PGF2a, not shown). Of the compounds tested which modulate PG and TX release from phagocytosing mouse peritoneal ...
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1038/274261a0
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 3
    Electronic Resource
    Electronic Resource
    On the metabolism of prostaglandins by rat brain homogenate (1976)
    Springer
    Cellular and molecular life sciences 32 (1976), S. 1114-1115 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary Using radio-immuno assays for prostaglandins and prostaglandin metabolites, three prostaglandin metabolizing enzymes were found in the 100,000×g supernatant of rat brain, 15-hydroxy-prostaglandin-dehydrogenase,Δ 13 and prostaglandin E-9-keto-reductase. Specific activity of the latter enzyme was highest in striatum and midbrain and lowest in cortex, cerebellum and spinal cord.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01927575
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 4
    Electronic Resource
    Electronic Resource
    Glucocorticoids: Effects on prostaglandin release, cyclic AMP levels and glycosaminoglycan synthesis in fibroblast tissue cultures (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 296 (1977), S. 131-137 
    Details
    ISSN: 1432-1912
    Keywords: Glucocorticoids ; PGE release ; Cyclic AMP levels ; Glycosaminoglycan synthesis ; Fibroblast cultures
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Glucocorticoids (GCs) reduced cyclic AMP levels and inhibited glycosaminoglycan (GAG) synthesis in secondary embryonic mouse fibroblast cultures, when cells were incubated for short periods (30 min). The order of potency was dexamethasone 〉 prednisolone 〉 hydrocortisone. The effect was more marked, when cyclic AMP levels and GAG synthesis were increased by addition of PGE1. Glucocorticoids exerted no longer an inhibitory effect on cyclic AMP and GAG synthesis in cultures pretreated for 48 h with the steroids. Addition of PGE1 caused a stronger rise in cyclic AMP and GAG synthesis than in controls without GC-preincubation. This enhancement was even more pronounced, when PGE1 was added together with the GCs. The reversal of the inhibitory effect of the GCs into a potentiating effect following preincubation correlated to a reduction of endogenous PGE formation in the cultures. Short-term treatment with GCs did not reduce endogenous PGE levels, but prolonged incubation markedly decreased PGE levels. PGE formation recovered following addition of fresh medium after the 48 h incubation with the steroids, but the amount of PGE formed remained significantly lower than in untreated cultures. Non-glucocorticoid steroid hormones did not decrease PGE levels. The results indicate that the apparent loss of inhibitory activity of GCs on cyclic AMP and GAG synthesis observed after prolonged incubation may result from a reduction of endogenous PGE formation which renders the cells more sensitive to the stimulatory effect of exogenous PGE1.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508464
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 5
    Electronic Resource
    Electronic Resource
    Radioimmunological determination of prostaglandin D2 synthesis in human thrombocytes (1978)
    Springer
    Cellular and molecular life sciences 34 (1978), S. 1494-1496 
    Details
    ISSN: 1420-9071
    Source: Springer Online Journal Archives 1860-2000
    Topics: Biology , Medicine
    Notes: Summary A specific radioimmunoassay for prostaglandin D2 was developed. Using the radioimmunoassay, prostaglandin D2 synthesis by human thrombocytes was measured. While the cyclooxygenase inhibitor indomethacin inhibits formation of prostaglandin D2, increased formation of prostaglandin D2 was observed in the presence of the thromboxane synthetase inhibitor imidazole.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01932373
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 6
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 7
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 8
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 9
    Electronic Resource
    Electronic Resource
    Bradykinin and postganglionic sympathetic transmission (1977)
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 299 (1977), S. 23-32 
    Details
    ISSN: 1432-1912
    Keywords: Bradykinin ; Prostaglandins ; Noradrenaline release ; Rabbit pulmonary artery ; Rabbit heart
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effect of bradykinin on postganglionic sympathetic neuroeffector transmission was studied in superfused strips of rabbit pulmonary artery and in perfused rabbit hearts. 1. In pulmonary artery strips preincubated with 3H-noradrenaline, bradykinin (1–100 nM) diminished the overflow of total tritiated compounds evoked by transmural stimulation at 2 Hz and simultaneously reduced stimulation-evoked contractions. The inhibition was stronger, the less time was allowed to elapse between addition of bradykinin and stimulation. The effect of bradykinin was not changed by atropine, but was abolished by indometacin and 5,8,11,14-eicosatetraynoic acid. 2. Separation of individual 3H-compounds showed that bradykinin and prostaglandin E2 (PGE2) caused proportionate reduction of the stimulation-evoked overflow of total radioactive material, 3H-noradrenaline, 3H-3,4-dihydroxyphenylglycol, and 3H-normetanephrine. 3. Bradykinin (1–100 nM) greatly increased the outflow of PGE from the tissue. The outflow peaked in the 3-min period after addition of bradykinin and then declined rapidly. PGF2α and the metabolites 15-keto-PGF2α, 13,14-dihydro-15-keto-PGF2α and 13,14-dihydro-15-keto-PGE2 were not detected. 4. In the heart, bradykinin (100 nM) diminished the overflow of endogenous noradrenaline evoked by sympathetic nerve stimulation at 3 Hz. Similar results were obtained in hearts perfused with atropine-containing medium. Indometacin, on the other hand, abolished the effect of bradykinin. 5. Bradykinin (100 mM) greatly increased the venous outflow of PGE. PGE2α and the metabolites 15-keto-PGF2α, 13,14-dihydro-15-keto-PGF2α and 13,14-dihydro-15-keto-PGE2 were not detected. 6. It is concluded that bradykinin inhibits the nerve impulse-evoked release of noradrenaline, and consequently postganglionic sympathetic neuroeffector transmission, by enhancing the biosynthesis of prostaglandins of the E series; however, a contribution to the inhibition by other products of the fatty acid cyclooxygenase pathway cannot be ruled out. No prostaglandin-independent presynaptic effect of bradykinin was found.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00508633
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
  • 10
    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
    Library Location Call Number Volume/Issue/Year Availability
    BibTip Others were also interested in ...
    Paper (German National Licenses)
    Fulltext
Close ⊗
This website uses cookies and the analysis tool Matomo. More information can be found here...