Literature DB >> 11280645

Reduction in intestinal leukocyte adherence in rat experimental endotoxemia by treatment with the 21-aminosteroid U-74389G.

C Lehmann1, A Georgiew, M Weber, J Birnbaum, W J Kox.   

Abstract

OBJECTIVES: To investigate leukocyte adherence in intestinal venules in experimental endotoxemia after treatment with the 21-aminosteroid U-74389G. DESIGN AND
SETTING: Prospective, randomized, controlled animal study in an experimental laboratory.
SUBJECTS: Twenty-one male Wistar rats weighing 190 +/- 40 g.
INTERVENTIONS: The rats were divided equally into three groups: (a) control group, (b) endotoxemia (5 mg/kg lipopolysacharide from Escherichia coli O55:B5), and (c) endotoxemia and U-74389G administration 30 min before (3 mg/kg) and 60 min after endotoxin challenge (1.5 mg/ kg).
MEASUREMENTS AND MAIN RESULTS: The distal small intestine of the animals was examined using intravital fluorescence videomicroscopy 2 h after endotoxin challenge. Leukocytes were stained in vivo by means of rhodamine 6G. In the endotoxemic animals we observed a fourfold increase in the count of firmly adherent leukocytes in submucosal post-capillary and collecting venules. Treatment with the 21-aminosteroid U-74389G significantly attenuated the count of sticking leukocytes in the collecting venules (control, 61 +/- 10 cells/mm2; lipopolysaccharide, 237 +/- 42 cells/mm2; U-74389G 125 +/- 9 cells/mm2; p < 0.05). In these venules leukocyte rolling behavior was comparable to that in the control group without endotoxin challenge.
CONCLUSIONS: Administration of U-74389G, which has radical scavenging properties, attenuates leukocyte adherence in selected populations of intestinal venules which is found increased during endotoxemia. Thus, 21-aminosteroids may have an impact in the treatment of endotoxin-induced intestinal injury.

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Year:  2001        PMID: 11280645     DOI: 10.1007/s001340000782

Source DB:  PubMed          Journal:  Intensive Care Med        ISSN: 0342-4642            Impact factor:   17.440


  1 in total

1.  Gu-4 suppresses affinity and avidity modulation of CD11b and improves the outcome of mice with endotoxemia and sepsis.

Authors:  TingTing Yan; Qing Li; HuiTing Zhou; YueTao Zhao; ShuQin Yu; GuangLin Xu; ZhiMin Yin; ZhongJun Li; ZhiHui Zhao
Journal:  PLoS One       Date:  2012-02-02       Impact factor: 3.240

  1 in total

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