rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2003-1-27
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pubmed:abstractText |
The terminal complement components play an important role in mediating tissue injury after ischemia and reperfusion (I/R) injury in rats and mice. However, the specific complement pathways involved in I/R injury are unknown. The role of the alternative pathway in I/R injury may be particularly important, as it amplifies complement activation and deposition. In this study, the role of the alternative pathway in I/R injury was evaluated using factor D-deficient (-/-) and heterozygote (+/-) mice. Gastrointestinal ischemia (GI) was induced by clamping the mesenteric artery for 20 minutes and then reperfused for 3 hours. Sham-operated control mice (+/- versus -/-) had similar baseline intestinal lactate dehydrogenase activity (P = ns). Intestinal lactate dehydrogenase activity was greater in -/- mice compared to +/- mice after GI/R (P = 0.02) thus demonstrating protection in the -/- mice. Intestinal myeloperoxidase activity in +/- mice was significantly greater than -/- mice after GI/R (P < 0.001). Pulmonary myeloperoxidase activity after GI/R was significantly higher in +/- than -/- mice (P = 0.03). Addition of human factor D to -/- animals restored GI/R injury and was prevented by a functionally inhibitory antibody against human factor D. These data suggest that the alternative complement pathway plays an important role in local and remote tissue injury after GI/R. Inhibition of factor D may represent an effective therapeutic approach for GI/R injury.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-10066708,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-10395324,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-10417391,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-10455904,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-10456004,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-10604887,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-10811844,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-11208721,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-11549596,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-11560858,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-11705901,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-11724962,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-11869678,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-11896391,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-11922743,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-12070223,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-12547694,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-2371562,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-266208,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-7805243,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-7840295,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-7981199,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-8642343,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-9631876,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12547703-9887056
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pubmed:language |
eng
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pubmed:journal |
|
pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
0002-9440
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
162
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
449-55
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:12547703-Animals,
pubmed-meshheading:12547703-Complement Factor D,
pubmed-meshheading:12547703-Complement Pathway, Alternative,
pubmed-meshheading:12547703-Kinetics,
pubmed-meshheading:12547703-L-Lactate Dehydrogenase,
pubmed-meshheading:12547703-Mice,
pubmed-meshheading:12547703-Mice, Knockout,
pubmed-meshheading:12547703-Peroxidase,
pubmed-meshheading:12547703-Rats,
pubmed-meshheading:12547703-Reperfusion Injury
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pubmed:year |
2003
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pubmed:articleTitle |
Role for the alternative complement pathway in ischemia/reperfusion injury.
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pubmed:affiliation |
Department of Anesthesiology, Perioperative, and Pain Medicine, Center for Experimental Therapeutics and Reperfusion Injury, Brigham and Women's Hospital, Harvard Medical School, Boston, Massachusetts 02115, USA. gstahl@zeus.bwh.harvard.edu
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pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
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