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在以往系列实验研究初步阐明头部重点低温具有多方面有利于脑复苏的生化机理的基础上，本文试图从细胞形态学方面予以佐证。应用新西兰白兔３２只，４只为正常对照（Ⅰ组），其余均用改良“四血管法”造成脑缺血（３０ｍｉｎ）模型，分为缺血对照（Ⅱ组）、常温再灌注（Ⅲ组）和头部重点低温（２８±０．５℃）再灌注（Ⅳ组）三组，Ⅲ、Ⅳ组再分为再灌注３０、１８０和３６０ｍｉｎ三亚组，每组各４只。处死后在体灌注固定液固定脑组织，将全脑作冠状切片制成常规石腊切片。采用计算机图像分析技术，将脑组织１２个部位的神经元按预定标准判为Ａ（正常）、Ｂ（轻伤）、Ｃ（重伤）和Ｄ（坏死）四类，予以分别计数和算出所占百分比。结果：Ⅱ组与Ⅰ组相比，Ａ类神经元所占百分比明显减少，Ｂ、Ｃ、Ｄ类明显增多；Ⅲ组Ａ、Ｂ类神经元进一步减少，而Ｃ、Ｄ类更显著增多；Ⅳ组Ａ、Ｂ类神经元所占百分比显著高于Ⅲ组，Ｄ类则明显减少，随着时间从３０～３６０ｍｉｎ，Ｃ、Ｄ类所占百分比基本恒定。结论：头部重点低温（脑温２８℃上下）对缺血后再灌注损伤具有明显的抑制作用，正常神经元得以免于受损。随着低温时间适当延长，轻伤神经元可能获救，而重伤和坏死神经元则无复苏可能。
Based on the previous series of experimental studies that tentatively elucidated the biochemical mechanism of head-key hypothermia in favor of brain resuscitation, this paper attempts to corroborate the findings in terms of cell morphology. Thirty-two New Zealand white rabbits were used, and the other four were normal control group (group Ⅰ). The rest were all treated with modified “four-vessel method” for 30 minutes. The rats were divided into two groups: ischemia control group Group Ⅲ) and Group Ⅲ (Ⅲ), Group Ⅳ (Group Ⅲ) with reperfusion at 28 ± 0.5 ℃ (Group Ⅳ) were further divided into three subgroups (30,180 and 360 min). After sacrifice in vivo perfusion fluid fixation of brain tissue, the whole brain for coronary slices made of conventional paraffin section. Using computer image analysis technology, the neurons in 12 parts of brain tissue were counted and calculated as A (normal), B (minor injury), C (severe injury) and D (necrosis) according to predetermined criteria percentage. Results: Compared with group Ⅰ, the percentage of neurons in group A decreased significantly, while those in group B, C and D increased significantly. The neurons in group A and B decreased further, while those in group C and D increased significantly. Group A, B neurons percentage was significantly higher than the group Ⅲ, D class was significantly reduced with the time from 30 ~ 360min, C, D percentage of the basic constant. Conclusion: The focal low temperature (28 ℃ above and below) can significantly inhibit the ischemia-reperfusion injury and prevent the normal neurons from being damaged. With the appropriate prolongation of low-temperature time, neurons may be rescued lightly injured, but there is no recovery of severely injured and necrotic neurons.