Open AccessRenal Function After Sevoflurane or Enflurane Anesthesia in the Fischer 344 Rat
Author(s) -
Malan Tp,
Yoshitami Kadota,
Heriberto P. Mata,
Frink Ej,
Brown Br
Publication year - 1993
Publication title -
anesthesia and analgesia/anesthesia and analgesia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.404
H-Index - 201
eISSN - 1526-7598
pISSN - 0003-2999
DOI - 10.1213/00000539-199310000-00028
Subject(s) - enflurane , sevoflurane , medicine , nephrotoxicity , anesthetic , excretion , anesthesia , isoflurane , inhalation , halothane , renal function , phenobarbital , pharmacology , kidney , endocrinology
Sevoflurane is metabolized to inorganic fluoride, a potential nephrotoxin. To evaluate the nephrotoxic potential of sevoflurane, 1-yr-old male Fischer 344 rats were anesthetized with 10 minimal alveolar anesthetic concentration (MAC) h sevoflurane or enflurane with or without pretreatment with biotransformation-enhancing agents. Peak serum fluoride levels reached 35 microM with sevoflurane anesthesia after pretreatment with phenobarbital and 40 microM after enflurane anesthesia after pretreatment with isoniazid. One day after anesthesia, sevoflurane-anesthetized rats concentrated urine normally in response to subcutaneous administration of 1-deamino-8-D-arginine vasopressin and exhibited no increase in urinary excretion of N-acetyl beta-glucosaminidase. Isoniazid-treated, enflurane anesthetized rats developed a 31% reduction in maximal urinary concentrating ability and a 3.5-fold increase in excretion of N-acetyl-beta-glucosaminidase. Sevoflurane produced no evidence of fluoride-induced nephrotoxicity in noninduced or enzyme-induced rats. Under similar conditions, enflurane produced laboratory evidence of nephrotoxicity.