缺血后适应减轻树鼩缺血性脑水肿及脑梗死的机制

目的 观察缺血后适应对树鼩血栓性脑缺血时大脑皮层脑水含量、局部脑血流、梗塞面积及神经元超微结构的影响，探讨其对树鼩脑缺血时神经保护的可能机制。 方法 将88只健康成年树鼩随机分为对照组、脑缺血4 h组、脑缺血24 h组、后适应4 h组及后适应24 h组（每组n=8）,另取8只动物做HE染色（n=3）及电子显微镜观察（n=5）。本实验采用光化学反应诱导树鼩血栓性脑缺血而建立脑缺血动物模型，在脑缺血模型建成后4 h夹闭缺血侧颈总动脉5 min，再灌注5 min，如此交替进行3个循环以建立缺血后适应模型。测定大脑皮层局部脑血流,脑组织含水量，脑梗死范围，并观察皮层及海马CA1区神经元超微结构改变。 结果 脑缺血时神经元固缩，线粒体肿胀，嵴溶解或形成空泡，内质网肿胀，内质网池形成。缺血后适应能使海马CA1区神经元固缩减少，线粒体和内质网的病理改变减轻，细胞水肿改善。随着缺血时间的延长，缺血24h组脑水含量明显增加86.81%±1.08%，此时脑梗塞面积明显扩大33.00%±3.03%，局部脑血流明显降低（134.27±28.75）ml/min。缺血后适应24h组脑组织含水量明显减少（81.04%±1.04%,P＜0.01）；脑梗塞面积缩小（16.79%±1.29%，P＜0.01）；而局部脑血流明显增加［（195.25±21.18）ml/min，P＜0.01］。 结论 缺血后适应可缓解树鼩缺血性脑水肿并缩小梗死范围，其机制可能与改善局部脑血流有关。

Mechanism of ischemic postconditioning relieved brain edema and cerebral infarction after cerebral ischemia in tree shrews

Objective To observe the effects of ischemic postconditioning (PC) on changes of cerebral water content,cerebral blood flow,infarct area and hippocampal ultrastructural,and to explore the neuroprotective mechanisms of ischemic PC on undergoing thrombotic cerebral ischemic injury.Methods Tree shrews were randomly grouped into control,ischemia 4 hours,ischemia 24 hours,ischemic postconditioning 4 hours and ischemic postconditioning 24 hours (n =8) Eight animals were used for HE staining(n =3) and electron microscopy(n =5).The model of thrombotic cerebral ischemia was induced by photochemistry in tree shrews.Four hours after the model establishment,the common carotid artery on the ischemia side was clamped for 5 minutes,then perfused by removing the clamp for 5 minutes,and repeated the same management 3 times,so that the model of PC was established.The changes of the brain water content of local cortex were measured by Elliott dry-wet weight and the brain infarct area was determind by 2,3,5-triphenyl-tetrazolium chloride staining.In addition,the regional cerebral blood flow of local cortex was measured by laser doppler,and the ultrastructural changes in the CA1 area of hippocampus in different groups were observed under an electron microscope.Results More neuron pycnosis was observed in hippocampal CA1 area.Obvious swelling of mitochondria,partial disrupt and vanish of the mitochondria cristae and more endoplasmic reticulum cisterna appeared in the neuron of hippocampus at the 24th hour after cerebral ischemia.With the time prolonging of ischemic,the brain water content was significantly increased (86.81％ ± 1.08％) in the ischemia group at the 24th hour compared with sham group.Cerebral infarction area was maximum (33.00％ ± 3.03％) and regional cerebral blood flow decreased obviously(134.27 ± 28.75) ml/min].The brain water content was significantly decreased (81.04％ ± 1.04％,P ＜ 0.01) and the infarct area was significantly shrink in ischemic postconditioning group (16.79％ ± 1.29％,P ＜ 0.01) than that in ischemia group.The regional cerebral blood flow in ischemic postconditioning group was in contrast to ischemia group significantly at the 24th hour (195.25 ± 21.18) ml/min,P ＜ 0.01].Conclusion Ischemic postconditioning attenuates the edema in ischemic brain and narrow the cerebral infarction area in tree shrews.The mechanism may be related to the improvement of local cerebral blood flow.