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  • 1
    Electronic Resource
    Electronic Resource
    Springer
    Naunyn-Schmiedeberg's archives of pharmacology 295 (1976), S. 237-241 
    ISSN: 1432-1912
    Keywords: Anaphylatoxin (C5a) ; Chemotaxis ; Leukocytes ; Vascular permeability ; Evans blue
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of highly purified hog anaphylatoxin (C5a) in leukocyte emigration were investigated in guinea pigs in vivo using two experimental models: 1. Subcutaneous infusions. Sterile solutions of C5a in saline infused at a rate of 1.8 μg C5a/h (0.2 ml/h) for 10h induced a dense accumulation of leukocytes, mainly neutrophils but also some eosinophils at the site of application. In control infusions with saline alone comparatively few leukocytes were found. 2. Single injections into the pleural cavity. 10 or 20 μg C5a (dissolved in 2 ml saline) caused a dosedependent increase in leukocyte number and volume of pleural exudate. Bradykinin in a dose of 18 μg produced similar fluid exudation as 20 μg C5a but had no significant effect on leukocyte accumulation. Intrapleural injections of C5a further caused the appearance of i.v. injected Evans blue in the pleural cavity. This effect, indicating an increase in vascular permeability lasted for about 3 h. Since at least one of the two models used — subcutaneous infusion—simulates natural conditions—continuous local generation of C5a in small amounts at the site of an inflammatory lesion—the results indicate that C5a once formed by complement activation in natural defense reactions may contribute to local increase in vascular permeability and leukocyte infiltration.
    Type of Medium: Electronic Resource
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  • 2
    ISSN: 1432-1912
    Keywords: Complement peptides ; Leukocytes ; Chemotaxis ; Vascular permeability ; Desensitization
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The effects of the spasmogenically active cleavage peptide from the third component of complement, C3a, and its spasmogenically inactive derivative, C3ai, on local leukocyte accumulation and vascular permeability in guinea pigs have been studied. 1. After intrapleural injection of 50, 100 or 150 μg both peptides induced a dose-dependent accumulation of leukocytes in the pleural cavity. This effect was significantly (P〈0.05) inhibited by colchicine (0.4 and 2.0 mg/kg), whereas pheniramine (5 mg/kg) and paramethasone (1 mg/kg) showed a slight inhibitory effect only. Indometacin (10 mg/kg) did not affect leukocyte accumulation. 2. C3a and C3ai also increased vascular permeability as shown by extravasation of i.v. applied Evans blue into the pleural cavity. This was partly inhibited by paramethasone and indometacin; pheniramine and colchicine were not inhibitory. When C3ai was injected intrapleurally (once 150 μg) and in addition intravenously (doses of 20, 100 and 150 μg injected every 20 min throughout the experiment), the accumulation of leukocytes in the pleural cavity was markedly decreased, whereas the extravasation of Evans blue was even increased. The inhibition of chemotaxis appears to be due to desensitization of the circulating leukocytes by the intravenously given C3ai thus rendering them unresponsive to the local stimulus of intrapleural C3ai. I.v. given C3ai induced a pronounced increase of the concentration of peripheral leukocytes.
    Type of Medium: Electronic Resource
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