Pentobarbital reduces rhabdomyolysis-induced acute renal failure in conscious rats.
BACKGROUND
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.


METHODS
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.


RESULTS
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.


CONCLUSIONS
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.
Subeq
Yi-Maun
YM
Institute of Medical Sciences, Department of Nursing, Tzu Chi University, Hualien, Taiwan.
Wu
Wen-Tien
WT
Lee
Chung-Jen
CJ
Lee
Ru-Ping
RP
Yang
Fwu-Lin
FL
Hsu
Bang-Gee
BG
D058186:Acute Kidney Injury / Q000209:etiology / Q000378:metabolism / Q000517:prevention & control*; D000818:Animals; D003071:Cognition / Q000502:physiology*; D004195:Disease Models, Animal; D005500:Follow-Up Studies; D018757:GABA Modulators / Q000008:administration & dosage / Q000627:therapeutic use*; D007150:Immunohistochemistry; D007275:Injections, Intravenous; D007684:Kidney Tubules / Q000378:metabolism / Q000473:pathology; D008297:Male; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000097:blood; D010424:Pentobarbital / Q000008:administration & dosage / Q000627:therapeutic use*; D051381:Rats; D017207:Rats, Sprague-Dawley; D012206:Rhabdomyolysis / Q000150:complications / Q000188:drug therapy* / Q000378:metabolism; D016896:Treatment Outcome
D018757:GABA Modulators; D016328:NF-kappa B; D010424:Pentobarbital