Free radical formation and high blood endotoxin levels are unlikely to be the primary causes of death in glycerol-induced fatal rhabdomyolysis in rats.
Challenges oxidative stress and endotoxemia as primary drivers of rhabdomyolysis mortality; hypothesis-generating for alternative mechanisms in animal models.
Rhabdomyolysis in experimental animals and in man may be fatal. The mechanism of action causing death in man and in the experimental model of laboratory animals injected with glycerol in a dose causing fatal rhabdomyolysis is unknown. The aim of this study was to examine two possible causes of death following glycerol injection (0.5-2 ml/100 g) to the leg muscle of rats following a period of water deprivation (24-72 h). The first factor examined was free radical formation, via the administration of various antioxidants such as natural antioxidant (NAO - 5 mg/100 g), vitamin E (0.2 mg/100 g each day for 7 days), dimethylthiourea (DMTU - 50 mg/100 g) and superoxide dismutase (SOD - 0.8 mg/100 g). The second factor was a high blood endotoxin level due to the glycerol injection. This possibility was examined by glycerol injection to rats that had developed endotoxin tolerance. The low survival rate (0-30%) of rats receiving a glycerol injection following preventive treatment with antioxidants as well as rats which had developed endotoxin tolerance (0-40%), excludes the possibility that the cause of death in the glycerol model resulting in fatal rhabdomyolysis is due to free radical formation or to a high and unneutralized blood level of endotoxin.
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Zurovsky et al. (1992) studied this question.
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