The Retino-Hypothalamic Ultrastructural Changes in Traumatic Optic Neuropathy

M. N.
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Abstract

Aim: To study the retino-hypothalamic ultrastructural changes in traumatic optic neuropathy’s pathogenesis and treatment. Methods: Four groups of mature rabbits were included in this experiment, 30 in each group, 120 in total. The traumatic crush to the optic nerves was reproduced by surgical clips to 90 mature rabbits. The first group (I) included intact/control animals, the second (II) included animals with traumatic optic neuropathy and two other traumatized groups (III and IV) who were given two different doses of treatment. The animals in group III were given infusions of Methylprednisolone 30mg/kg/day for three days. The group IV animals received infusion of 15mg/kg/ day of Methylprednisolone for 3 days in combination with phosphine electric stimulation (PES), starting from the third until the 13th day of the experiment. The electrical pulse which was used on the affected side of the animal was 800 mА and 300 mА on the opposite side. The morphological analysis of the retina and suprachiasmatic nucleus of the hypothalamus of all the four groups of animals included electron microscopy of the semi-thin and ultrathin sections. This analysis was performed a month following the initial injury while the animals were removed from the experiment. The levels of cortisol and adrenocorticotropic hormone (ACTH) in the blood of all experimental animals was tested up to one month following the injury to the optic nerves. Results: We found that trauma to the orbital part of the optic nerve causes collocative necrosis of ganglion cells and swelling of the nerve fiber layer of the ipsilateral retina. In addition, such traumatic damage causes structural changes in the suprachiasmatic nucleus of the hypothalamus. Combined treatment of methylprednisolone with phosphine electro stimulation in traumatized rabbits reduced the thickness of the retina, reduced the cytokaryometric indices and the regeneration processes of bipolar and ganglion cells of the retina. Histopathologically we found an increased number of neurosecretory granules in the suprachiasmatic nucleus of the hypothalamus. ACTH levels in the blood of the group III rabbits were found to be lower, while the cortisol levels higher, and these hormone levels in the IV group rabbits were quite similar to those of the group which was not treated. Conclusion: The combined treatment of traumatic optic neuropathy in rabbits with phosphine electrostimulation and methylprednisolone can be considered a useful treatment, having a beneficial neuroprotective effect.
外伤性视神经病变视网膜-下丘脑超微结构改变
目的:探讨外伤性视神经病变的视网膜-下丘脑超微结构变化。方法:选用4组成年家兔,每组30只,共120只。用手术夹复制90只成年兔的视神经外伤。第一组(I)包括完整/对照动物,第二组(II)包括创伤性视神经病变动物,另外两个创伤组(III和IV)给予两种不同剂量的治疗。III组给予甲基强的松龙30mg/kg/d,连续3 d。IV组动物从实验第3 ~第13天开始,连续3 d注射甲基强的松龙15mg/kg/ d,并联合磷化氢电刺激(PES)。在动物患病侧使用的电脉冲为800 mÐ′,对侧使用的电脉冲为300 mÐ′。四组动物视网膜和下丘脑视交叉上核的形态学分析包括半薄和超薄切片的电镜观察。这项分析是在最初受伤一个月后进行的,当时动物被移出实验。在视神经损伤后一个月检测所有实验动物血液中的皮质醇和促肾上腺皮质激素(ACTH)水平。结果:视神经眶部损伤引起同侧视网膜神经节细胞坏死和神经纤维层肿胀。此外,这种创伤性损伤引起下丘脑视交叉上核的结构改变。甲基强的松龙联合磷化氢电刺激治疗损伤家兔视网膜厚度降低,细胞核指数降低,视网膜双极细胞和神经节细胞再生过程减慢。组织病理学上,我们发现下丘脑视交叉上核的神经分泌颗粒数量增加。III组家兔血液中ACTH水平较低,皮质醇水平较高,而IV组家兔的这些激素水平与未治疗组相当。结论:磷化氢电刺激联合甲基强的松龙治疗兔外伤性视神经病变是一种有效的治疗方法,具有良好的神经保护作用。
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