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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 22 (1987), S. 202-208 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract Intravenous injection of ellagic acid (EA, 30 mg/Kg), an activator of the Hageman factor, induced congestion of lymph nodes and dilatation of the spleen in rats. The dilatation of the spleen was inhibited by heparin, thrombin, defibrase, clocoumarol. lambda carrageenan, SBTI, PCR 4099 and CCI 17810. The congestion of lymph nodes was inhibited by heparin, thrombin, defibrase, clocoumarol, SBTI, lambda carrageenan, aspirin, indomethacin and ketoprofen, phentolamine and hexamethonium. Thrombin, defibrase, lambda carrageenan did not induce any congestion of the lymphoid tissues. These results suggest that the dilatation of the spleen induced by ellagic acid would result from blood coagulation, platelet stimulation and kinin formation. The congestion of lymph nodes would depend on kinins, blood coagulation and prostaglandins. The activation of Hageman factor in acute inflammatory reactions could mediate the early congestion of lymph nodes.
    Type of Medium: Electronic Resource
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  • 2
    Electronic Resource
    Electronic Resource
    Springer
    Inflammation research 22 (1987), S. 270-279 
    ISSN: 1420-908X
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Abstract We compared the major changes induced by ellagic acid (EA), a Hageman factor activator, in normal rats and in kininogen-deficient Brown Norway rats. In normal rats, large doses of EA induced a congestion of lymph nodes, spleen and liver, a prolongation of activated partial thromboplastin time, the consumption of prekallikrein, high molecular weight kininogen and fibrinogen, as well as the stimulation of platelets with their accumulation in lungs, liver and spleen. A systemic hypotension of long duration was also observed. The fibrinogen consumption, the thrombocytopenia and the lengthening of activated partial thromboplastin time were dose-dependent. In kininogen-deficient rats, EA induced only a minimal congestion of lymphoid tissues, the accumulation of platelets in lungs, a decrease of plasma fibrinogen and a short-lasting hypotension. It is concluded that the vascular changes induced by blood coagulation with ellagic acid resulted mainly from kinin formation.
    Type of Medium: Electronic Resource
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  • 3
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 325 (1984), S. 76-79 
    ISSN: 1432-1912
    Keywords: Kinins ; Urate crystals ; Uric acid ; Inflammation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary 1. Monosodium urate and uric acid crystals induced kinin formation in Wistar rat plasma. They were inactive in the Brown Norway rat plasma which did not contain high molecular weight kininogen and had a low level in prekallikrein. 2. Crystal-induced inflammation in the Brown Norway rat paw developed later and reached only 70% of the values observed in Wistar rats. Captopril, a kininase inhibitor, enhanced the oedema induced in the Wistar rat but did not affect the oedema in the Brown Norway rat. The leucocyte accumulation in the peritoneal cavity afte uric acid injection was similar in both strains. 3. The kinin system appeared to be involved in the inflammatory process induced in the rat by urate and uric acid crystals, as it is involved in carrageenan oedema.
    Type of Medium: Electronic Resource
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