Effects of sevoflurane on neuronal cell damage after severe cerebral ischemia in rats.

Department of Anesthesiology and Pain Medicine, Seoul National University Hospital, Seoul, Korea.
Korean journal of anesthesiology 10/2011; 61(4):327-31. DOI: 10.4097/kjae.2011.61.4.327
Source: PubMed

ABSTRACT The aim of this study was to investigate the neuroprotective effects of sevoflurane after severe forebrain ischemic injury. We also examined the relationship between the duration of ischemia and neuronal cell death.
Male Sprague-Dawley rats (300-380 g) were subjected to 6 (each n = 6) or 10 min (each n = 10) of near-complete forebrain ischemia while anesthetized with either 50 mg/kg of zoletil given intraperitoneally or inhaled sevoflurane (2.3%). Ischemia was induced by bilateral common carotid artery occlusion plus hemorrhagic hypotension (26-30 mmHg). Histologic outcomes were measured 7 days after ischemia in CA1 pyramidal cells of the rat hippocampus.
The mean percentage of necrotic cells in the hippocampal CA1 area decreased in the sevoflurane group compared to the zoletil group (25% vs. 40% after 6 min ischemia, respectively: P = 0.004 and 44% vs. 54% after 10 min of ischemia, respectively P = 0.03). The percentage of apoptotic cells was similar in all groups. The percentage of necrotic cells in each anesthetic groups was significantly higher in the 10 min ischemia group compared to the 6 min ischemia group (P = 0.004 in the sevoflurane group, P = 0.03 in the zoletil group).
The present data show that sevoflurane has neuroprotective effects in rats subjected to near-complete cerebral ischemia. Longer duration of ischemia is associated with more neuronal injury when compared to ischemia of shorter duration.

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    Korean journal of anesthesiology 10/2011; 61(4):273-4.
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    ABSTRACT: BACKGROUND: /st>The purpose of this study was to investigate whether combined administration of celecoxib and sevoflurane after ischaemia produces additive neuroprotection against transient global cerebral ischaemia in rats. METHODS: /st>Cerebral ischaemia was induced by bilateral common carotid artery occlusion with haemorrhagic hypotension for 8 min. After ischaemia, no drugs were administered in the sham (n=4) and control (n=10) groups. In the celecoxib group (n=10), celecoxib 2 mg kg(-1) was administered after reperfusion. In the sevoflurane group (n=10), after reperfusion, sevoflurane 2.4% was inhaled two times for 5 min each at an interval of 10 min to achieve postconditioning. In the celecoxib+sevoflurane group (n=10), administration of celecoxib 2 mg kg(-1) and the sevoflurane postconditioning were performed simultaneously. Necrotic or apoptotic cells were examined in the hippocampus 7 days after ischaemia. Serum levels of proinflammatory cytokines including tumour necrosis factor-α and interleukin-1β were measured 2 h, and 3 and 7 days after ischaemia. RESULTS: /st>Necrotic or apoptotic cells were observed more frequently in the control group than in the celecoxib or sevoflurane groups 7 days after ischaemia (P<0.05). Cytokine levels were higher in the control group when compared with the celecoxib or sevoflurane groups 2 h after ischaemia (P<0.05). However, the histological outcomes and cytokine levels were similar in all three groups treated with celecoxib or sevoflurane. CONCLUSIONS: /st>Combined treatment with celecoxib and sevoflurane after global cerebral ischaemia has no additive neuroprotective effects in rats.
    BJA British Journal of Anaesthesia 02/2013; · 4.24 Impact Factor


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