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目的：观察犬电击致室颤心脏停跳（ＶＦＣＡ）８分钟复苏后脑亚低温（３３℃）对脑脊液（ＣＳＦ）、脑组织中超氧化物歧化酶（ＳＯＤ）活力、丙二醛（ＭＤＡ）含量和脑皮质神经元超微结构的影响。方法：对犬行ＶＦＣＡ８分钟，开胸心肺复苏后观察４小时。１０只犬分为２组：正常脑温心肺复苏组（ＮＴ组，ｎ＝４）维持硬脑膜外温度３６～３７℃；选择性脑亚低温心肺复苏组（ＳＢＣ组，ｎ＝６）采用右侧颈总动脉灌注自体血冷却辅以头部表面降温维持硬脑膜外温度３３℃左右。结果：ＮＴ组复跳后各时点ＣＳＦ中ＳＯＤ活性较ＣＡ前均明显降低（Ｐ均＜０．０５），ＭＤＡ含量则均明显升高（Ｐ均＜０．０５），神经元核膜、线粒体、内质网等结构严重受损；ＳＢＣ组与ＮＴ组相比则复跳后各时点ＣＳＦ和脑组织中ＳＯＤ活性均明显升高（Ｐ均＜０．０５），ＭＤＡ含量均明显降低（Ｐ均＜０．０５），神经元超微结构损害明显减轻。结论：脑亚低温（３３℃左右）可能通过抑制脑内脂质过氧化反应和内源性氧自由基清除剂的消耗，对脑复苏起到有利的保护作用。
OBJECTIVE: To observe the changes of superoxide dismutase (SOD) and malondialdehyde (MDA) contents in cerebrospinal fluid (CSF) and brain tissue after cerebral thaw hypothermia (33 ℃) and 8 min after VFCA Effect of Ultrastructure of Cerebral Cortical Neurons. Methods: VFCA was performed in dogs for 8 minutes and after 4 hours of cardiopulmonary resuscitation after thoracotomy. Ten dogs were divided into two groups: normal epicardial CPR group (NT group, n = 4) maintained epidural temperature 36-37 ℃; selective cerebral mild hypothermia cardiopulmonary resuscitation group (SBC group, n = 6) Side of the common carotid artery perfusion with autologous blood cooling head surface cooling to maintain the epidural temperature of about 33 ℃. Results: Compared with the pre-CA level, the activity of SOD in the CSF of the NT group was significantly decreased (P <0.05) and the content of MDA was significantly increased (P <0.05) Mitochondria, endoplasmic reticulum and other structures were severely damaged. Compared with NT group, the activity of SOD in CSF and brain tissue of SBC group was significantly increased (P <0.05) and MDA content was significantly decreased (All P <0.05), the ultrastructural damage of neurons was significantly reduced. Conclusion: Mild hypothermia (about 33 ℃) may play a beneficial protective effect on cerebral resuscitation by inhibiting lipid peroxidation in the brain and depletion of endogenous oxygen free radical scavengers.