It is not easy to detect oxygen free radicals directly because of thei
r very short half-life. In the present study, a sensitive ultraweak ch
emiluminescence detector was used to detect the generation of oxygen f
ree radicals following thermal injury. Twelve New Zealand white rabbit
s were used in this study. After anesthesia, the bilateral hind-limbs
were exposed to 100 degrees C water for 30 s. Six control animals were
exposed to 22 degrees C water to act as a control. The chemiluminesce
nce of whole blood and visceral organs were measured with both luminol
-amplified t-butyl hydroperoxide-initiated and lucigenin-initiated met
hods. The results showed that chemiluminescence of blood was affected
significantly by acute thermal injury. The chemiluminescence of blood
increased significantly at 1 h following acute thermal injury, reached
a peak at 2 h, then decreased but still remained above the control le
vel at 4 h following thermal injury. The results for TBHP-initiated ch
emiluminescence from visceral organs following acute thermal injury we
re much higher than that of the control rabbits. The effects of lucige
nin-initiated tissue chemiluminescence following acute thermal injury
were not statistically significant. It is suggested that the decreased
vascular antioxidant activity following local thermal injury is parti
ally contributed by the superoxide pathway; while, the remote pathophy
siologic events are mediated by the defective scavenging defenses. (C)
1998 Elsevier Science Ltd for ISBI. All rights reserved.