[Hepatic dysfunction in myoglobinuric acute renal failure (rhabdomyolysis)--experimental study in rats]

Liver damage as a consequence of rhabdomyolysis (RM) has not been well established on clinical and experimental grounds. Hepatic dysfunction was then investigated in rats 24 h after induction of acute renal failure with glycerol. Forty male Wistar rats (220-270 g) were dehydrated for 24 h and were divided in two group: GI experimental group (n = 14)-50% glycerol was injected (10 ml/Kg, one-half of the dose in each hindlimb muscle) and GII control group (n = 26)-animals received injection of saline solution. Twenty-four hours after the glycerol or saline injection all the animals were killed. Serum urea, creatinine, transaminases (AST, ALT) and CK were measured and significantly high values were obtained in experimental animals. Arterial blood pressure was measured and remained within normal levels in both groups. Hepatocyte mitochondrial respiratory function was estimated polarographically with determination of oxygen consumption without ADP (Basal respiration-State 4) and in the presence of ADP (Activated respiration-State 3). In experimental group (GI) there was significant low values of oxygen consumption in state 3, decrease of respiratory control rate and in ADP/O ratio (p < 0.05). Histological studies of the liver revealed a periportal necrosis and centrilobular degeneration. These studies suggested that hepatic dysfunction is an additional complication of glycerol-induced rhabdomyolysis. The pathogenesis and clinical implications of these abnormalities are discussed.