中华实验外科杂志
中華實驗外科雜誌
중화실험외과잡지
CHINESE JOURNAL OF EXPERIMENTAL SURGERY
2012年
6期
1141-1142
,共2页
预吸氧%线粒体%脑%缺氧复氧性损伤
預吸氧%線粒體%腦%缺氧複氧性損傷
예흡양%선립체%뇌%결양복양성손상
Preoxygenation%Mitochondria%Brain%Hypoxia reoxygenation injury
目的 观察预吸氧对缺氧复氧性脑损伤时大脑皮质线粒体的影响.方法 在大鼠脑缺氧复氧前20 min预吸氧30 min,测定脑皮质线粒体膜流动性和超微结构的变化.结果 大鼠缺氧/复氧后线粒体结构和功能均有所损伤,表现为线粒体膜流动性降低(微黏度η和各向异性γ由2.505±0.837、0.182±0.032分别增高到4.801±0.531、0.242±0.009,P<0.01)和超微结构变化,预吸氧能明显加重这种损伤(微黏度η和各向异性γ分别进一步增高到6.217±1.598、0.270±0.017),其机制与抑制三磷酸腺苷(ATP)敏感性钾通道有关.结论 预吸氧能加重缺氧复氧性脑损伤.
目的 觀察預吸氧對缺氧複氧性腦損傷時大腦皮質線粒體的影響.方法 在大鼠腦缺氧複氧前20 min預吸氧30 min,測定腦皮質線粒體膜流動性和超微結構的變化.結果 大鼠缺氧/複氧後線粒體結構和功能均有所損傷,錶現為線粒體膜流動性降低(微黏度η和各嚮異性γ由2.505±0.837、0.182±0.032分彆增高到4.801±0.531、0.242±0.009,P<0.01)和超微結構變化,預吸氧能明顯加重這種損傷(微黏度η和各嚮異性γ分彆進一步增高到6.217±1.598、0.270±0.017),其機製與抑製三燐痠腺苷(ATP)敏感性鉀通道有關.結論 預吸氧能加重缺氧複氧性腦損傷.
목적 관찰예흡양대결양복양성뇌손상시대뇌피질선립체적영향.방법 재대서뇌결양복양전20 min예흡양30 min,측정뇌피질선립체막류동성화초미결구적변화.결과 대서결양/복양후선립체결구화공능균유소손상,표현위선립체막류동성강저(미점도η화각향이성γ유2.505±0.837、0.182±0.032분별증고도4.801±0.531、0.242±0.009,P<0.01)화초미결구변화,예흡양능명현가중저충손상(미점도η화각향이성γ분별진일보증고도6.217±1.598、0.270±0.017),기궤제여억제삼린산선감(ATP)민감성갑통도유관.결론 예흡양능가중결양복양성뇌손상.
Objective To investigate the effects of preoxygenation on the structure and function of cerebral cortex mitochondria in rats subject to hypoxia-reoxygenation injury.Methods At 20 min before hypoxia,the rats were given rpreoxygenation for 30 min.The mitochondrial membrane fluidity was assayed and the ultrastructural changes of mitochondria were observed under the electron microscopy.Results The brain mitochondrial membrane fluidity was decreased (η and γ were 4.801 ±0.531 and 0.242 ±0.009 respectively) after hypoxia-reoxygenation (η and γ were 2.505 ± 0.837 and 0.182 ± 0.032 respectively,all P<0.01 ).Preoxygcnation ean increase the brain mitochondrial membrane fluidity increase sequentially (η and γ were 6.217 ± 1.598 and 0.270 ± 0.017 ).The effects of preoxygenation on hypoxia-reoxygenation brain injury were realized by inhibiting the activity of brain adenosine triphosphate (ATP)-sensitive potassium channel.Conclusion Preoxygenation can aggravate the brain injury of hypoxia-reoxygenation.