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Postconditioning with isoflurane reduced ischemia-induced brain injury in rats.
- Source :
-
Anesthesiology [Anesthesiology] 2008 Jun; Vol. 108 (6), pp. 1055-62. - Publication Year :
- 2008
-
Abstract
- Background: Preexposure of brain to isoflurane, a commonly used anesthetic, induces ischemic tolerance. This phenomenon is called isoflurane preconditioning. However, it is not known whether isoflurane application after ischemia provides neuroprotection.<br />Methods: Corticostriatal slices (400 microm) freshly prepared from adult male Sprague-Dawley rats were subjected to a 15-min oxygen-glucose deprivation (OGD; to simulate ischemia in vitro). Isoflurane was applied after OGD. Brain slices were harvested 2 h after OGD for measuring 2,3,5-triphenyltetrazolium chloride (TTC) conversion to quantify cell injury. Adult male Sprague-Dawley rats were also subjected to middle cerebral arterial occlusion for 90 min and then treated with or without 2% isoflurane for 60 min started at the onset of reperfusion. The infarct volumes, neurologic deficit scores, and performance on rotarod were evaluated at 24 h after the onset of reperfusion.<br />Results: Isoflurane applied immediately after the 15-min OGD for 30 min dose-dependently reversed the OGD-induced decrease of TTC conversion. The TTC conversion was 34 +/- 16% and 58 +/- 28% of the control, respectively, for OGD alone and OGD plus 2% isoflurane (P < 0.05, n = 12). Application of 2% isoflurane for 30 min started at 10 min after the OGD also reduced the OGD-decreased TTC conversion. The presence of 0.3 microm glibenclamide, a general adenosine 5'-triphosphate-sensitive potassium channel blocker, or 500 microm 5-hydroxydecanoic acid, a mitochondrial adenosine 5'-triphosphate-sensitive potassium channel blocker, during the application of 2% isoflurane abolished the isoflurane preservation of TTC conversion. Application of isoflurane during reperfusion also improved neurologic outcome after brain ischemia.<br />Conclusions: The results suggest that isoflurane administrated after OGD or brain ischemia provides neuroprotection. Mitochondrial adenosine 5'-triphosphate-sensitive potassium channels may be involved in this protection.
- Subjects :
- Animals
Brain drug effects
Decanoic Acids pharmacology
Dose-Response Relationship, Drug
Glyburide pharmacology
Hydroxy Acids pharmacology
Hypoxia-Ischemia, Brain etiology
Hypoxia-Ischemia, Brain pathology
Infarction, Middle Cerebral Artery complications
Male
Middle Cerebral Artery drug effects
Organ Culture Techniques
Potassium Channel Blockers pharmacology
Rats
Rats, Sprague-Dawley
Reperfusion Injury prevention & control
Tetrazolium Salts metabolism
Tetrazolium Salts pharmacokinetics
Anesthetics, Inhalation pharmacology
Brain blood supply
Hypoxia-Ischemia, Brain prevention & control
Isoflurane pharmacology
Neuroprotective Agents pharmacology
Subjects
Details
- Language :
- English
- ISSN :
- 1528-1175
- Volume :
- 108
- Issue :
- 6
- Database :
- MEDLINE
- Journal :
- Anesthesiology
- Publication Type :
- Academic Journal
- Accession number :
- 18497606
- Full Text :
- https://doi.org/10.1097/ALN.0b013e3181730257