To investigate the relationship between the inflammatory responses and postresuscitation syndrome, we prospectively examined the serial changes of
neutrophil elastase (NE),
urinary trypsin inhibitor (UTI), and
TNF-alpha) in successfully resuscitated patients after
out-of-hospital cardiac arrest. This study included 36 patients with
out-of-hospital cardiac arrests who were admitted to our intensive care unit after return of spontaneous circulation (ROSC). The 11 patients who restored to spontaneous circulation within 30 min after
cardiac arrest were defined as the short
cardiac arrest group. The 25 patients who restored to spontaneous circulation more than 30 min after
cardiac arrest were defined as the long
cardiac arrest group. Eight healthy volunteers served as control group. Daily plasma levels of NE, UTI, and
TNF-alpha were measured from days 1 to 5 after ROSC. The releases of NE from activated neutrophil just after ROSC in the patients with long
cardiac arrest were statistically higher than those of the short
cardiac arrest group. There was a significant correlation between the NE levels and the duration of
cardiac arrest. A high but insufficient production of UTI for NE release was observed on day 1, especially in the patients with a long duration of
cardiac arrest. The cerebral performance category of the short
cardiac arrest group was better than that of the long
cardiac arrest group. Although high levels of
TNF-alpha were sustained in the postresuscitation period, the levels of
TNF-alpha were unrelated to the duration of
cardiac arrest. In conclusion, a massive release of NE in proportion to the duration of
cardiac arrest and an insufficient production of UTI for the NE release may contribute to the pathogenesis of postresuscitation syndrome after
out-of-hospital cardiac arrest.