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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
1994-1-14
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pubmed:abstractText |
C plays a critical role in the hyperacute rejection (HAR) of discordant xenografts (Xg), but the relative contribution of early vs late C components is unknown. In this study, genetic differences in C6 activity were correlated with HAR of guinea pig cardiac Xg by the rat. Seven rat strains were tested for C activity. Six strains (PVG.R1 (R1), PVG.1A (1A), DA, W/F, F344, LEW) had readily detectable C activity in the total and alternative pathways. Some PVG rats also had adequate C activity [PVG (C+)] but others [PVG (C-)] had a profound C6 deficiency. All rats with adequate C activity (n = 35) rejected cardiac Xg between 15 and 80 min. PVG (C+) (n = 6) rats also rejected cardiac Xg hyperacutely (26 +/- 12 min), whereas PVG (C-) (n = 16) rats, which had high preformed IgM natural antibody titers, rejected cardiac Xg in 1 to 2 days (2678 +/- 542 min). Transfer of serum from R1 rats to PVG (C-) recipients with vigorously beating Xg caused HAR of cardiac Xg within 116 +/- 75 min. Transfer of fresh PVG (C-) serum or heat-inactivated R1 serum did not induce HAR. HAR was characterized by intravascular platelet aggregation and interstitial hemorrhage, whereas Xg transplanted to PVG (C-) recipients had patent vessels at 30 min but were heavily infiltrated by granulocytes and monocytes at 2 days. These findings indicate that a deficiency in C6 prevents HAR but allows an accelerated acute rejection that may be mediated by the generation of vasoactive and chemotactic C3a and C5a.
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pubmed:grant | |
pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
151
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
7240-8
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pubmed:dateRevised |
2007-11-14
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pubmed:meshHeading |
pubmed-meshheading:8258722-Animals,
pubmed-meshheading:8258722-Complement C3,
pubmed-meshheading:8258722-Complement C5,
pubmed-meshheading:8258722-Complement C6,
pubmed-meshheading:8258722-Complement Hemolytic Activity Assay,
pubmed-meshheading:8258722-Complement Pathway, Alternative,
pubmed-meshheading:8258722-Cricetinae,
pubmed-meshheading:8258722-Graft Rejection,
pubmed-meshheading:8258722-Heart Transplantation,
pubmed-meshheading:8258722-Immunoglobulin M,
pubmed-meshheading:8258722-Kinetics,
pubmed-meshheading:8258722-Male,
pubmed-meshheading:8258722-Myocardium,
pubmed-meshheading:8258722-Rats,
pubmed-meshheading:8258722-Rats, Inbred Strains,
pubmed-meshheading:8258722-Transplantation, Heterologous
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pubmed:year |
1993
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pubmed:articleTitle |
Use of C6-deficient rats to evaluate the mechanism of hyperacute rejection of discordant cardiac xenografts.
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pubmed:affiliation |
Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205.
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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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