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Original Articles
- The Effects of Mild Hypothermia on the Expression of the Apoptosis-related Proteins following Transient Global Ischemia in Gerbil Hippocampus
- Young Min Kim, Kyu Nam Park, Seung Pil Choi, Tai Yong Hong, Se Kyung Kim
- Korean J Crit Care Med. 2007;22(1):30-41.
- 1,699 View
- 19 Download
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Abstract
PDF - BACKGROUND
The neuroprotective mechanisms of hypothermia remain unclear. Recently, attenuation of apoptosis by hypothermia has been suggested as one of the responsible mechanisms. The aim of this study is to investigate the effects of post-ischemic hypothermia on apoptotic neuronal death as well as expression of some apoptosis-related proteins in a gerbil transient global ischemia model.
METHODS
Following 5 minutes of ischemia, normothermia (NT, 37+/-0.5degrees C) or mild hypothermia (HT, 33+/-0.5degrees C) was immediately induced and maintained for 3 hours. The hippocampal CA1 neurons were examined on day 2, 3, 4, and 7 after ischemia for the survived neuronal densities, DNA nick end labeling and immunohistochemical expressions of Bcl-2, Bax, and caspase 3 in each group. Additionally, DNA gel electrophoresis and western blot analysis for each protein in hippocampus were performed. RESULTS: The neuronal death in CA1 area on day 3, 4, and 7 was significantly reduced in HT group compared to NT group. The number of TUNEL positive cells in HT group was also significantly reduced than NT group on day 3, 4, and 7. DNA laddering of hippocampus on day 4 and 7 also reduced in HT group. Expressions of Bax on days 2, 3 and activated caspase 3 on days 3, 4 were reduced in HT group. Western blots also disclosed a decrease in the intensity of the Bax on day 2 and 3 in HT group compared to NT group. CONCLUSIONS: These results suggest that mild post-ischemic hypothermia attenuates the apoptotic neuronal death through the inhibition of the intrinsic pathway of caspase activation following transient global ischemia and these effects may be related to a reduction of pro-apoptotic events.
- Effects of Sevoflurane and Ischemic Preconditioning on Neurologic Injury and Bcl-2 Family Protein mRNA Expression after Transient Spinal Ischemia in the Rats
- Soon Hwan Kang, Eun Soo Kim, Seung Hoon Baek, Jae Young Kwon
- Korean J Crit Care Med. 2004;19(1):20-31.
- 1,376 View
- 6 Download
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Abstract
PDF
- BACKGROUND
Spinal cord injury occurring as the result of surgical repair of thoracic and thoracoabdominal aortic disease remains a devastating complication. Anesthetic and ischemic preconditioning have been known to prevent ischemic injury. The purpose of this study was to elucidate the effects of sevoflurane and ischemic preconditioning (IPC) on neurologic outcome, DNA fragmentation and Bcl-2 protein gene expression in transient spinal ischemia. METHODS: Rats were anesthetized with enflurane or sevoflurane, divided by 5 groups: Sevoflurane group and enflurane group (13 minutes of ischemia), Control group, Rapid group, Delayed group (15 minutes of ischemia). Spinal ischemia was produced by both induced hypotension and thoracic aortic cross clamping. Neurologic scores were assessed at the time of recovery and 1, 2, 3, 24 hours after transient spinal ischemia. After 24 hours, rats were euthenized and spinal cords were removed for the assay of DNA fragmentation. Other groups of rats received 5 minutes of ischemia, and after 1, 6, 24, 48 and 72 hours, spinal cords were removed for the assay of Bcl-2 family protein mRNA and DNA fragmentation. RESULTS: The neurologic injury and DNA fragmentation of sevoflurane group were significantly lesser than enflurane group. 5 minutes of IPC caused increase in Bcl-xl protein mRNA transcription at 48 and 72 hours reperfusion. There were no significant changes in neurologic injury, Bcl-2 family mRNA transcription and DNA fragmentation between control group, rapid group, and delayed group. CONCLUSIONS: Sevoflurane was effective in preventing neurologic injury after 13 minutes of transient spinal ischemia. However, rapid and delayed ischemic preconditioning did not potentiated neuroprotective action of sevoflurane during 15 minutes of spinal ischemia.
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