Article

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.

  • Source

    Full-text · Article · Oct 2011 · Korean journal of anesthesiology
  • Source
    [Show abstract] [Hide abstract]
    ABSTRACT: Background: 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: 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: 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: Combined treatment with celecoxib and sevoflurane after global cerebral ischaemia has no additive neuroprotective effects in rats.
    Preview · Article · Feb 2013 · BJA British Journal of Anaesthesia
  • [Show abstract] [Hide abstract]
    ABSTRACT: We previously showed that preischemic administration of high-dose isoflurane worsened the outcome from severe forebrain ischemia in rats. Conversely, high doses of sevoflurane have been reported to improve the outcome from forebrain ischemia when the insult is moderate. To clarify the dose-dependent effects of sevoflurane on severe forebrain ischemia, we performed an outcome study using an identical protocol to that in our previous study with isoflurane. Fasting male Sprague-Dawley rats underwent surgical preparation for forebrain ischemia under halothane anesthesia. Anesthesia was changed to fentanyl/nitrous oxide to eliminate the halothane, after which 30 minutes of 0.5, 1.0, 1.5, 2.0, or 2.5 minimum alveolar concentration sevoflurane was administered. Ten minutes of ischemia was induced by bilateral carotid occlusion plus systemic hypotension, in which cessation of electroencephalographic activity was confirmed. Sevoflurane was discontinued and anesthesia continued with fentanyl/nitrous oxide for an additional 100 minutes. Outcome evaluation at 5 days postischemia included seizure incidence, mortality rate, neuromotor score, and histologic injuries to the cerebral cortex and hippocampal CA1 and CA3. Different doses of sevoflurane did not statistically affect seizure incidence (10.0% to 18.2%), mortality rate (20.0% to 46.7%), cortical damage (mild to moderate degree), or hippocampal CA1 damage (93.7% to 96.7% neuronal necrosis) or CA3 damage (36.3% to 41.7%). Dose-dependent effects of sevoflurane were not observed for any of the outcome variables assessed in this rat model of severe forebrain ischemia.
    No preview · Article · Nov 2014 · Journal of Neurosurgical Anesthesiology
Show more