To investigate the role of
oxygen-derived
free radicals in the pathogenesis of
tourniquet shock, the authors present an experimental animal model. Two groups of rats were fastened with rubber tubes on both thighs (1.5 kg/cm2) for 6 h under
pentobarbital anaesthesia. One group was administered liposomal
superoxide dismutase (L-SOD 30,000 U/kg
body weight), and the other
liposome as a control 3 h prior to
tourniquet removal. No rats in the control group (n = 20) survived more than 24 h after reperfusion, whereas 55% of animals treated with L-SOD (n = 20) survived for 24 h or more, and two recovered completely (P less than 0.005). Blood samples were obtained from the abdominal aorta after
laparotomy of anaesthetized rats of both groups at different time intervals. Changes in the hematocrit value and blood
urea nitrogen during the early periods after reperfusion were attenuated by prior administration of L-SOD, and the total plasma SOD activity of the control animals decreased promptly and continuously throughout the experimental period. This experimental model was very useful to study the pathogenesis of
tourniquet shock with respect to reproducibility, induction of the
shock stages and mortality. It is thought that
oxygen-
free radicals are involved in the induction of
tourniquet shock, and L-SOD was, to a certain extent, effective against
reperfusion injury in the early stages of
shock.