Objective      To study the role of IL-18 and its relation with superoxide anion production and hydroxyl free radical released from neutrophils in rat resuscitation model following burn shock.       Methods      At 6

12

24 and 48 h after a rat resuscitation model following burn shock was established

the peripheral IL-18 level was measured and the number of neutrophils in the blood sample was calculated. The number of superoxide free radicals and hydroxy free radicals in neutrophils of the rat model was calculated after intraperitoneal injection with IL-18 (20 g/kg) and anti-rat-IL-18 antibody (80 μg/kg). The freshly isolated neutrophils were cultured in vitro

into which IL-18 (0.5 μg/ml) and anti-rat-IL-18 antibody (0.5 μg/ml) were added. The number of superoxide free radicals and hydroxy free radicals in neutrophils was calculated in 24 h after culture.       Results      The level of peripheral IL-18 (51.46±11.36

64.86±12.05

78.64±15.64 and 69.44±12.28 pg/ml) and the number of peripheral neutrophils [(38.46±13.57)×10

5

/ml

(128.45±45.78)×10

5

/ml

(245.25±84.15)×10

5

/ml and (179.56±49.27)×10

5

/ml

]

were significantly higher in resuscitation group than in control group at 6

12

24 and 48 h after burn (P0.01). The superoxide anion and 8-OHdG levels were significantly higher in rats injected with IL-18 than in those with sham burn (0.45±0.03 vs 0.15±0.02

605±145 vs 152±21

605±145 vs 152±21 pg/ml

P0.01) and significantly lower in rats injected with anti-rat-IL-18 antibody than in those after delayed resuscitation (0.19±0.03 vs 0.32±0.04

198±45 vs 524±124 pg/ml

P0.01). The superoxide anion and 8-OHdG levels were significantly higher in neutrophils into which IL-18 was added than in those into which IL-18 was not added (0.38±0.02 vs 0.13±0.02

505±99  vs 92±21 pg/ml

P0.01) and significantly lower in rats injected with anti-rat-IL-18 antibody than in those with burn (0.16±0.03 vs 0.2

9±0.04

95±45 vs 324±68 pg/ml

P0.01).       Conclusion      IL-18 can effectively bind to neutrophils in rats during delayed resuscitation and promote production of superoxide free radicals in rat resuscitation model following burn shock

thus leading to further tissue damage.