Pentobarbital reduces rhabdomyolysis-induced acute renal failure in conscious rats

Rhabdomyolysis is one of the causes of acute renal failure. Pentobarbital enhances the action of gamma-aminobutyric acid and suppresses the activities of nuclear factor (NF)-kappaB pathways. In this study, we used pentobarbital to study the effects on the glycerol-induced rhabdomyolysis with acute renal failure in conscious rats.

Rhabdomyolysis was induced by intramuscular injection of 10 mL/kg of 50% glycerol in conscious rats. Ten minutes later, the rats received an intravenous injection of pentobarbital (10 mg/kg in 0.5 mL/h normal saline) or normal saline (0.5 mL/h). Biochemical substances, including blood urea nitrogen (BUN), creatinine (Cre), glutamic oxaloacetic transaminase (GOT), glutamic pyruvic transaminase (GPT), and creatine phosphokinase (CPK) were measured at 0 hour, 1 hour, 3 hours, 6 hours, 12 hours, 24 hours, and 48 hours. Rats were killed by decapitation at 48 hours after glycerol administration, and the kidneys were removed immediately for pathological findings and immunohistochemistry.

Intramuscular injection of glycerol significantly increased blood BUN, Cre, GOT, GPT, CPK levels and induced severe histopathologic damage in the kidneys. NF-kappaB and inducible nitric oxide synthase (iNOS) were increased, and E-cadherin was decreased after glycerol administration, as detected by immunohistochemistry in the kidneys. Posttreatment with pentobarbital decreased blood BUN, Cre, GOT, GPT, CPK levels, decreased the markers of kidney injury, and suppressed the release of NF-kappaB and iNOS after rhabdomyolysis.

Posttreatment with pentobarbital suppressed the activities of NF-kappaB and iNOS, decreased BUN, Cre, GOT, GPT, CPK levels, and decreased the markers of kidney injury after rhabdomyolysis. These actions ameliorated rhabdomyolysis-induced acute renal failure in conscious rats.