期刊
JOURNAL OF INFECTIOUS DISEASES
卷 198, 期 2, 页码 271-274出版社
OXFORD UNIV PRESS INC
DOI: 10.1086/589514
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资金
- NHLBI NIH HHS [R01 HL058837-10, R01 HL081326-01A2, HL58837, R01 HL058837, HL81326, R01 HL081326, R01 HL058837-11] Funding Source: Medline
Anticoagulation is a rational approach to the treatment of sepsis-associated consumptive coagulopathy, but its application is limited because of the risk of excessive bleeding. Factor XI (FXI) contributes substantially to pathological blood coagulation ( thrombosis), whereas it contributes only modestly to normal hemostasis. We found that FXI-deficient mice have reduced coagulopathy and increased survival relative to FXI-expressing wild-type mice during cecal ligation and puncture induced acute peritonitis/sepsis. This finding suggests that FXI contributes to coagulopathy and/or inflammation during sepsis and that pharmacologic inhibition of FXI activity may alter the course and outcome of some infections.
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