Kabakuş N, Ozcan A, Aysun S, Yilmaz B
Department of Pediatric Neurology, Firat University, Faculty of Medicine, Elaziğ, Turkey.
Cell Biochem Funct. 2006 May-Jun;24(3):257-60. doi: 10.1002/cbf.1214.
This study was undertaken to investigate the effects of neonatal cerebral hypoxic-ischaemic brain injury (HIBI) in acute and early chronic phases in the rat. HIBI was induced in 7-day-old rat pups by ligation of the right common carotid and then the pups were exposed to 1 h of hypoxia in 8% oxygen. They were divided into two groups: 1-day (acute phase, in the first 24 h) and 5-day (early chronic phase, 120 h). Neuropathological evaluation was performed using the hippocampus, cerebral cortex and basal ganglia on the coronal plane. The following values were obtained: (i) the ratio of the infarcted area; (ii) hemispheric atrophy/asymmetry; (iii) patchy lesions confined to the thalamus, caudate and putamen; (iv) the ratio of damaged neurons to all neurons; and (v) the percentage of apoptotic neurons relative to the total neurons in all brain areas. HIBI-induced global cerebral damage and cellular damage findings did not significantly differ between the two groups. However, they showed a tendency to recover/deteriorate in both acute and early chronic phases. The ratio of ipsi- and contra-lateral hemisphere infarct areas (20.7 and 15.7% vs. 40.1 and 26.7%, respectively), basal ganglia patchy lesion ratio (27.5 vs. 36.7%) and hemispheric atrophy/asymmetry (92.4 vs. 84.7%) were found to be lower in the rat pups in the chronic phase than those in the acute phase. In contrast, increases in the ratio of damaged neurons (16.7 vs. 13.3% in the cerebral and dorsal hippocampus, respectively) and in the ratio of apoptotic neurons (ipsi-lateral: 18 vs. 6%; contra lateral hemispheres: 3.5 vs. 1.7%, respectively) were recorded. It is concluded that cellular damage tends to deteriorate (damaged and apoptotic neurons) while global damage (cerebral infarct and patchy damage) improves with the progression of HIBI. However, further studies are needed in order to elucidate this process.
本研究旨在探讨新生大鼠急性和早期慢性阶段脑缺氧缺血性脑损伤（HIBI）的影响。通过结扎7日龄大鼠幼崽的右侧颈总动脉诱导HIBI，然后将幼崽置于8%氧气环境中缺氧1小时。它们被分为两组：1天组（急性期，前24小时）和5天组（早期慢性期，120小时）。在冠状面上使用海马体、大脑皮层和基底神经节进行神经病理学评估。获得了以下数值：（i）梗死面积比例；（ii）半球萎缩/不对称性；（iii）局限于丘脑、尾状核和壳核的斑片状病变；（iv）受损神经元与所有神经元的比例；（v）所有脑区凋亡神经元相对于总神经元的百分比。两组之间HIBI诱导的全脑损伤和细胞损伤结果无显著差异。然而，它们在急性和早期慢性阶段均呈现恢复/恶化的趋势。发现慢性期大鼠幼崽同侧和对侧半球梗死面积比例（分别为20.7%和15.7% vs. 40.1%和26.7%）、基底神经节斑片状病变比例（27.5% vs. 36.7%）和半球萎缩/不对称性（92.4% vs. 84.7%）低于急性期。相反，记录到受损神经元比例增加（大脑和背侧海马体分别为16.7% vs. 13.3%）以及凋亡神经元比例增加（同侧：18% vs. 6%；对侧半球：3.5% vs. 1.7%）。结论是随着HIBI的进展，细胞损伤（受损和凋亡神经元）趋于恶化，而全脑损伤（脑梗死和斑片状损伤）有所改善。然而，需要进一步研究以阐明这一过程。
