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Dose-Dependent Influence of Sevoflurane Anesthesia on Neuronal Survival and Cognitive Outcome After Transient Forebrain Ischemia in Sprague-Dawley Rats
Background Volatile anesthetics reduce postischemic neurohistopathological injury and improve neurological outcome in various animal models. However, the isoflurane concentrations above 1 minimum alveolar concentration (MAC) have been associated with reduced neuronal survival and impaired functional...
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Published in: | Neurocritical care 2011-12, Vol.15 (3), p.577-584 |
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Main Authors: | , , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | Background
Volatile anesthetics reduce postischemic neurohistopathological injury and improve neurological outcome in various animal models. However, the isoflurane concentrations above 1 minimum alveolar concentration (MAC) have been associated with reduced neuronal survival and impaired functional outcome. The aim of this study was to evaluate if 1.8 MAC sevoflurane alters postischemic neuronal survival and neurologic outcome compared with 0.45 MAC sevoflurane.
Methods
In this study, 20 fasted male Sprague-Dawley rats were randomly assigned to treatment groups with 1 or 4 vol.% sevoflurane end-tidal concentration. Cerebral ischemia was induced by bilateral carotid artery occlusion and hemorrhagic hypotension (BCAO). The cognitive outcome was assessed after 7 days using the object recognition test. Animals were then re-anesthetized and brains were removed for neurohistopathological analysis of the hippocampus (CA1) and cortex using hematoxylin-eosin staining.
Results
Physiologic parameters were not different between both the treatment groups. The number of viable neurons (median [Q1, Q3]) in the CA1 region on postischemic day 7 was increased after high-dose sevoflurane compared with low-dose sevoflurane (1645 [453, 1825] vs. 3222 [2920, 3993] neurons/ROI,
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ISSN: | 1541-6933 1556-0961 |
DOI: | 10.1007/s12028-011-9562-3 |