摘要
目的:应用离体大鼠海马脑片电生理记录技术,观察七氟烷对海马脑片在缺氧过程中突触后诱发群峰电位(PS)的时相以及复氧后幅度变化的影响,探讨七氟烷对脑组织缺氧损伤的保护作用。方法:实验于2004-09/12在徐州医学院江苏省麻醉学重点实验室电生理研究室进行。大鼠乙醚麻醉后迅速断头取脑,低温分离海马,并沿矢状面将其切成0.5mm厚的脑片。实验分为缺氧组和七氟烷(1%,2%和4%)处理组。平衡灌注后,双脉冲方波刺激海马CA3区Schaffer侧支,记录海马CA1区锥体细胞的诱发群峰电位潜伏期和幅度作为基础值,所有取得基础值的脑片分别按上述分组进行实验。用通入95%N2和5%CO2混合气的人工脑脊液灌注脑片,实施缺氧,时间为5min。更换通入人工脑脊液的混合气为95%O2和5%CO2,实施复氧,时间120min。七氟烷在缺氧前10min给予,并维持在缺氧期间和复氧后10min,给药时间为25min。实验结束后各组取脑片四五片用TTC染色,酶标仪测定A490值,与空白对照值比较,分析脑片活性。结果:①与基础值相比,2%七氟烷可明显延长正常脑片诱发群峰电位出现的潜伏期(P<0.05),不降低诱发群峰电位幅度;4%的七氟烷不延迟诱发群峰电位出现的潜伏期,但可显著降低诱发群峰电位的幅度(P<0.05)。②与缺氧组相比,2%和4%七氟烷均明显延迟缺氧所致的诱发群峰电位消失时间(P<0.05);而4%七氟烷又可明显增加复氧后诱发群峰电位幅度的恢复率(P<0.05),降低脑片TTC染色下降百分率,差异有显著性意义(P<0.05)。结论:4%七氟烷可明显延迟海马脑片缺氧所致诱发群峰电位消失的时间,增加复氧后诱发群峰电位幅度的恢复率,具有抗缺氧损伤的神经保护作用。
AIM： To observe the effect of sevoflurane on phase of evoked postsynaptic population spikes （PS） after hypoxia and the changes of range of PS after given oxygen in rat hippocampal slices with electrical physiological recording technigue, and explore the protective effect of sevoflurane on hypoxic injury of cerebral tissue. METHODS： The experiment was conducted at the research room of electrophysiology, Jiangsu Provincial Key Laboratory of Anesthesiology, Xuzhou Medical College from September to December 2004, Brain was got after anesthesia with diethyl ether. Hippocampus was separated under hypothermia and was cut into 0.5 mm brain slices along the sagittal plane. There were hypoxia group and sevoflurane group （1%, 2% and 4%）, After equilibrium perfusion, stimulating electrodes were placed on Schaffer collateral fibers at hippocampal CA3 region with double impulse square wave and the evoked postsynaptic population spikes were recorded from the CA1 pyramidal cell layer of the rat hippocampal slice. Latency and range were recorded as basic value, All the cerebral slices that got basic value were treated with the experiment according to the above mentioned group, respectively, Man-made cerebrospinal fluid that had given 95%N2 and 5%CO2 mixture gas was used to fill cerebral slices, performing hypoxia for 5 minutes. And then the mixture gas was changed into 95%02 and 5% CO2, giving oxygen for 120 minutes. Ten minutes before hypoxia, the sevoflurane was given and maintained for 10 minutes in hypoxia and after giving oxygen. Administration time was 25 minutes. Four to five cerebral slices were got after experiment and stained with TTC. A490 value was detected with enzyme-marked meter, and compared with the blank control value. Activity of cerebral slice was analyzed. RESULTS： ①As compared with the basic value, the 2% sevoflurane significantly increased the latency but did not significantly decrease the amplitude of the postsynaptic spike before hypoxia. 4% sevoflurane did not prolong the latency of the postsynaptic population spike, but could reduce the amplitude of the postsynaptic population spike （P 〈 0.05）. ②As compared with the hypoxia group, 2% and 4% sevoflurane obviously prolong the disappeared time of the postsynaptic population spike due to hypoxia （P 〈 0.05）. While 4% sevoflurane could obviously increase the recovery rate of the amplitude of the postsynaptic population spike after giving oxygen （P 〈 0.05）, decrease the percentage of decrease of TFC staining of cerebral slices, which had significant difference （P 〈 0.05）. CONCLUSION： 4% sevoflurane can significantly delay the disappeared time of evoked postsynaptic population spikes induced by hypoxia of cerebral slices of hippocampus, increase the recovery rate of the amplitude of the postsynaptic population spike after giving oxygen and have the neural protective effect on anti-hypoxia injury.
出处
《中国临床康复》
CSCD
北大核心
2006年第2期91-93,共3页
Chinese Journal of Clinical Rehabilitation
