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Insufficient production of urinary trypsin inhibitor for neutrophil elastase release after cardiac arrest

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Title: Insufficient production of urinary trypsin inhibitor for neutrophil elastase release after cardiac arrest
Other Titles: Insufficient production of urinary trypsin inhibitor for elastase release promotes organ failure following cardiac arrest
Authors: Hayakawa, Mineji Browse this author →KAKEN DB
Sawamura, Atsushi Browse this author
Yanagida, Yuichiro Browse this author
Sugano, Masahiro Browse this author
Kubota, Nobuhiko Browse this author
Hoshino, Hirokatsu Browse this author
Gando, Satoshi Browse this author
Keywords: ischemia
protease inhibitor
tumor necrosis factor-α
Issue Date: May-2008
Publisher: Lippincott Williams & Wilkins
Journal Title: Shock
Volume: 29
Issue: 5
Start Page: 549
End Page: 552
Abstract: To investigate the relationship between the inflammatory responses and post-resuscitation syndrome, we prospectively examined the serial changes of neutrophil elastase (NE), urinary trypsin inhibitor (UTI) and tumor necrosis factor-α (TNF-α) in successfully resuscitated patients following out-of-hospital cardiac arrest. This study included 36 patients with out-of-hospital cardiac arrests that wewere admitted to our intensive care unit after return of spontaneous circulation (ROSC). The twenty-two patients who died within 3 days after ROSC were defined as nonsurvivors. The fourteen patients who survived for more than 3 days after ROSC were defined as survivors. Eight healthy volunteers served as control group. Daily plasma levels of NE, UTI, and TNF-α were measured from days 1 to 5 after ROSC. Persistently high levels of TNF-α and NE were observed in both the survivors and nonsurvivors. In the two groups, the levels of UTI were significantly high and increased as time progressed. NE/UTI ratios were significantly higher in the nonsurvivors than in the survivors, especially on day 1. The nonsurvivors showed statistically higher scores according to the Sequential Organ Failure Assessment and they also had more organ failure than the survivors. In conclusion, an insufficient production of UTI for NE release and persistent high levels of TNF-α may contribute to the pathogenesis of post-resuscitation syndrome following out-of-hospital cardiac arrest.
Rights: This is a non-final version of an article published in final form in Shock. 29(5):549-552, May 2008
Type: article (author version)
Appears in Collections:北海道大学病院 (Hokkaido University Hospital) > 雑誌発表論文等 (Peer-reviewed Journal Articles, etc)

Submitter: 早川 峰司

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