| The Effects of Propofol and Sevoflurane on Neuronal Apoptosis and Bcl-2 Family Protein Expression after Transient Forebrain Ischemia in the Rat. |
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Byoung Gyu Ahn, Won Sung Kim, Jae Young Kwon |
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Department of Anesthesiology and Pain Medicine, Pusan National University College of Medicine, Busan, Korea. jykwon@pusan.ac.kr |
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| Abstract |
BACKGROUND
Anesthetic preconditioning and anesthetics itself have been known to prevent ischemic injury in brain and heart. The purpose of this study was to evaluate the effects of anesthetics and anesthetic preconditioning on neuronal apoptosis and Bcl-2 family protein expression in transient forebrain ischemia.
METHODS
Rats were divided into 3 groups and anesthetized with intraperitoneal propofol (P group) or sevoflurane (S and SP groups). In SP group, rats were anesthetized with sevoflurane during 30 minutes and then anesthesia was maintained with intraperitoneal propofol. Forebrain ischemia was produced by both induced hypotension and 10 minutes of common carotid artery clamping.
RESULTS
At 2 days after ischemia, the numbers of necrotic cells in hippocampal CA1 area in S group were less than P and SP groups, and the number of apoptotic cells in S and SP groups were less than P group. The expressions of Bcl-xl in P and SP groups were less than S group. The expression of Bax in P group was less than S and SP groups. At 2 weeks after ischemia, the numbers of necrotic cells in hippocampal CA1 area in S and SP groups were less than P group, and the numbers of apoptotic cells in S group were less than P and SP groups. The expressions of Bcl-xl in S group were more than P and SP groups.
CONCLUSIONS
Sevoflurane could reduce ischemic injury during transient forebrain ischemia. However the anesthetic preconditioning with sevoflurane could not help to prevent delayed neuronal apoptosis after forebrain ischemia. |
| Key Words:
apoptosis; Bcl-2; brain ischemia; propofol; rat; sevoflurane |
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