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Isoflurane exerts a short‐term but not a long‐term preconditioning effect in neonatal rats exposed to a hypoxic‐ischaemic neuronal injury
Author(s) -
SASAOKA N.,
KAWAGUCHI M.,
KAWARAGUCHI Y.,
NAKAMURA M.,
KONISHI N.,
PATEL H.,
PATEL P. M.,
FURUYA H.
Publication year - 2009
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.2008.01822.x
Subject(s) - isoflurane , medicine , anesthesia , neuroprotection , hippocampus , ischemia , pharmacology
Background: Isoflurane has been shown to induce tolerance against ischaemic injury in adult rodents. Although the delayed preconditioning effect of isoflurane has been demonstrated in neonatal rat pups, the acute preconditioning effects of isoflurane remained undetermined. The present study was therefore conducted to evaluate the acute preconditioning efficacy of isoflurane in neonatal rats subjected to a hypoxic‐ischaemic (HI) injury. Methods: Post‐natal day 7 pups were exposed to 1 or 2% isoflurane in oxygen for either 30, 60 or 90 min. Fifteen minutes after isoflurane exposure, the pups were subjected to an HI injury induced by left common carotid artery ligation and exposure to 8% oxygen for 2 h. Pups not exposed to isoflurane or not subjected to HI served as controls. Histopathologic injury to the cortex and hippocampus was evaluated 7 and 49 days after HI. Results: Isoflurane 2% exposure for 60 or 90 min before HI induced tolerance in the hippocampus and the number of normal neurons in the CA1 sector 7 days after HI was significantly greater than in non‐preconditioned animals. This protective efficacy of isoflurane preconditioning was not observed 49 days after HI. Conclusions: Exposure of 2% isoflurane for at least 60 min is required to induce tolerance against HI injury in rat pups. However, this neuroprotective efficacy results in only transient neuroprotection.