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  • Prostaglandins  (3)
  • 6-keto-PGF1α  (1)
  • Eiosanoids  (1)
  • 1
    Electronic Resource
    Electronic Resource
    Congenital nephrogenic diabetes insipidus — vasopressin and prostaglandins in response to treatment with hydrochlorothiazide and indomethacin (1987)
    Springer
    Pediatric nephrology 1 (1987), S. 485-490 
    Details
    ISSN: 1432-198X
    Keywords: Hydrochlorothiazide ; Indomethacin ; Nephrogenic diabetes insipidus ; Prostaglandins ; Vasopressin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract In four boys with congenital nephrogenic diabetes insipidus, plasma arginine-vasopressin (AVP) and urinary excretion of prostaglandins were studied in response to treatment with hydrochlorothiazide and indomethacin. An abnormal relationship between AVP and urine osmolality was demonstrated in all patients. In the first patient, treatment with indomethacin (3 mg/kg per day) resulted in a drop of the inulin and paraminohippurate clearances. In the other three patients urinary excretion of PGE2 was raised, and fell during treatment with hydrochlorothiazide (2 mg/kg per day) and indomethacin (2 mg/kg per day). Urine flow, free water clearance and osmolar clearance decreased during treatment. A combination of both drugs is more effective than hydrochlorothiazide alone and the effect appears to be additive.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00849258
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    Paper (German National Licenses)
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  • 2
    Electronic Resource
    Electronic Resource
    The role of eicosanoids in paediatrics (1988)
    Springer
    European journal of pediatrics 147 (1988), S. 341-349 
    Details
    ISSN: 1432-1076
    Keywords: Eiosanoids ; Prostaglandins ; Modulation ; Mediation ; Early life
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Prostanoids are unsaturated cyclic fatty acids, are synthesized primarily from arachidonic acid, and, like the leukotrienes, belong to the growing family of eicosanoids. As tissue hormones, prostanoids act on specific receptors near their site of synthesis and degradation. Prostanoids operate as modulators and mediators in a large spectrum of physiological processes. They are involved in the regulation of maternal and fetal circulation, patency of the ductus arteriosus, plateletvessel wall interaction and kidney function. Besides their physiological function in protecting organ perfusion under stress conditions, they are also involved in diseases as described in the hyperprostaglandin E2-syndrome or — together with leukotrienes-in inflammatory processes. More specific pharmacological tools than the nonsteroidal antiinflammatory drugs, such as receptor antagonists, selective synthesis inhibitors, and eicosanoid analogues offer the prospect of enriching our arsenal of pharmacotherapeutic interventions in a variety of diseases. Before active intervention, however, more and specific biochemical analyses are required to identify the pathophysiological role of eicosanoid.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00496408
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    Paper (German National Licenses)
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  • 3
    Electronic Resource
    Electronic Resource
    Determination of peripheral plasma prostanoid concentration: An unreliable index of ‘in vivo’ prostanoid activity (1986)
    Springer
    European journal of clinical pharmacology 31 (1986), S. 303-305 
    Details
    ISSN: 1432-1041
    Keywords: prostanoid concentrations ; plasma ; gas chromatography/mass spectrometry ; PGE2 ; PGF2α ; 6-keto-PGF1α ; TxB2
    Source: Springer Online Journal Archives 1860-2000
    Topics: Chemistry and Pharmacology , Medicine
    Notes: Summary Plasma concentrations of PGE2, PGF2α, 6-keto-PGF1α and TxB2 were determined in 4 healthy volunteers by gas chromatography-negative ion chemical ionization mass spectrometry. TxB2 concentrations in all volunteers increased with time during blood collection, increases occurred more sporadically in the case of PGE2, PGF2α and 6-keto-PGF1α. Rapid changes in plasma prostanoid concentrations within a sampling series were unpredictable and were inexplicable. The measured plasma prostanoid concentrations apparently depended on the sampling conditions, which could not be adequately standardized and controlled. However, very short term changes in plasma prostanoid levels cannot be excluded.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00981128
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    Paper (German National Licenses)
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  • 4
    Electronic Resource
    Electronic Resource
    Prostaglandin-mediated hypercalcemia: A paraneoplastic syndrome (1978)
    Springer
    Journal of molecular medicine 56 (1978), S. 373-387 
    Details
    ISSN: 1432-1440
    Keywords: Prostaglandine ; Hypercalcämie ; Knochenresorption ; paraneoplastische Hypercalcämie ; Parathormon ; Prostaglandins ; Hypercalcemia ; Bone resorption ; Neoplastic endocrine-like syndrome ; Parathyroid hormone
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Description / Table of Contents: Summary Evidence has been presented for prostaglandin-mediated hypercalcemia and bone resorption in malignancies of both, experimental animals and man. Occurrence of hypercalcemia in cancer patients is known for a long time, but its pathogenesis has been poorly understood so far. Besides ectopic parathyroid hormone secretion by tumors, an osteoclastactivating factor released from leukocytes and direct bone destruction by tumor cells, prostaglandins of the E series have to be considered as one of the candicates involved in the pathomechanism of hypercalcemia and osteoclastic osteolysis in cancer patients. This new concept on the pathophysiology of cancer-associated hypercalcemia has implications for the diagnosis and management of this common complication of neoplastic disease.
    Notes: Zusammenfassung Es liegen sowohl tierexperimentelle als auch klinische Studien vor, die auf eine Beteiligung der Prostaglandine bei der Entstehung der paraneoplastischen Hypercalcämie und Knochenresorption hinweisen. Das Syndrom der paraneoplastischen Hypercalcämie ist bereits seit längerem bekannt, jedoch ist ihre Pathogenese nur unzureichend aufgeklärt. Neben dem ektopisch sezernierten Parathormon, dem leukozytär gebildeten Osteoklasten-aktivierenden Faktor und der direkten Knochenzerstörung durch Tumorzellen muß Prostaglandinen der E-Serie eine wesentliche Rolle im Pathomechanismus der paraneoplastischen Hypercalcämie und der osteoklastären Osteolyse eingeräumt werden. Dieses neue Konzept zur Pathophysiologie der Hypercalcämie bei Karzinomträgern hat wesentliche Folgen für die Diagnostik und Therapie dieser häufigen Komplikation neoplastischer Erkrankungen.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF01477292
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    Paper (German National Licenses)
    Fulltext
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