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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4h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24 h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24 h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。
Objective To observe the effects of post-ischemic postconditioning on cerebral water content, regional cerebral blood flow, infarct size and neuronal ultrastructure during cerebral ischemia in tree shrews, and to explore its neuroprotective potential during cerebral ischemia in tree shrews mechanism. Methods Eighty healthy adult tree shrews were randomly divided into control group, cerebral ischemia 4 h group, cerebral ischemia 24 h group, postconditioning 4 h group and postconditioning 24 h group (n = 8 in each group), another 8 Only animals were HE stained (n = 3) and electron microscopy (n = 5). In this experiment, we used photochemical reaction to induce cerebral ischemia in tree shrews to establish a model of cerebral ischemia. After occlusion of the ischemic common carotid artery for 5 min and reperfusion for 5 min after cerebral ischemia model was established, 3 Circulation to establish an ischemic postconditioning model. The cerebral cortex regional cerebral blood flow, water content of brain tissue and infarct size were measured. The ultrastructural changes of cortical and hippocampal CA1 neurons were observed. Results Neuronal pyknosis, swelling of mitochondria, cristae dissolved or vacuolated, endoplasmic reticulum swelling and endoplasmic reticulum formation were observed during cerebral ischemia. Post-ischemic postconditioning can reduce neuronal pyknosis in hippocampal CA1 region, mitigate the pathological changes of mitochondria and endoplasmic reticulum, and improve cell edema. With the prolongation of ischemic time, the brain water content in ischemic group increased significantly by 86.81% ± 1.08% at 24 h, the area of cerebral infarction was significantly increased by 33.00% ± 3.03%, and the local cerebral blood flow was significantly decreased by 134.27 ± 28.75 ml / min. The cerebral water content in ischemic postconditioning group decreased significantly (81.04% ± 1.04%, P <0.01), the area of cerebral infarction was reduced (16.79% ± 1.29%, P <0.01), while the local cerebral blood flow increased significantly 195.25 ± 21.18) ml / min, P <0.01]. Conclusions Post-ischemic postconditioning can alleviate ischemic brain edema and reduce the infarct size in tree shrews. The mechanism may be related to the improvement of local cerebral blood flow.