عنوان مقاله [English]
نویسندگان [English]چکیده [English]
Inhalant anaesthetics are used widely for producing general anaesthesia in animals and humans.. Approximately 20% of halothane uptake is metabolised via oxidative and reductive pathways during and following halothane anaesthesia in humans. Fifteen clinically healthy dogs were assigned in three groups (group 1, 2and 3) randomly. All dogs were anesthetized with halothane three times that was repeated 48 hours after the first anesthesia in all groups. Dogs in group one, two and three anesthetized for one, three and five hours respectively. All anesthesia were repeated every 48 hours as totally three anesthesia (D1, D2, and D3) were performed in each group. Jugular blood samples were obtained in 0 (before anesthesia), 1, 3, 5 and 24 hours after induction of anesthesia for measurement of BUN and Creatinin concentration. 72 hours after anesthesia, animals were euthanized and kidneys were removed for histopathological evaluation. No significant differences were observed in serum BUN and Creatinin concentration in group 1 in different sampling times compared with time 0 during study. In group 2 and 3 serum BUN and Creatinin were increased 3,5 and 24 hours compared to group 1 in third anesthesia (D3)(P<0.05).In group 3 serum BUN and Creatinin were increased 1 hours after anesthesia compared to group 1 and group 2 in third anesthesia(D3) (P<0.05). Microscopic findings revealed that there were not any pathological changes in group 1. However, kidneys of animals in group 2 and 3 were affected with acute tubular necrosis (ATN), medullary congestion and glomerular atrophy. Basement membrane of tubules with ATN appeared normal and necrotic cells were sloughed into the tubular lumens. The significant difference of BUN and Creatinin among the experiment groups revealed that long duration halothane anesthesia might be resulted in renal damage, decreased glomerular filtration rate and increased BUN and Creatinin.