Kalkan Erdal, Eser Olcay, Avunduk Mustafa Cihat, Coşar Murat, Fidan Hüseyin, Kalkan Serpil
Department of Neurosurgery, Selçuk University, Meram Medicine Faculty, 42080 Akyokuş, Konya, Turkey.
Ulus Travma Acil Cerrahi Derg. 2006 Oct;12(4):263-7.
Apoptosis is a process of programmed cell death that plays a role in some normal and pathological conditions. In this study, we investigated the apoptosis during cerebral ischemic reperfusion injury in response to haemorrhagic shock in a rat model.
Thirty-six adult Sprague-Dawley rats were divided into six groups: control, haemorrhagic shock (HS), ischemic reperfusion (IR), 1st hour IR, 3rd hour IR, 6th hour IR and 24th hour IR. Rats were sacrificed by taking blood from intracardiac area after finishing the experiment. The tissues were fixed using neutral buffered 10% formaldehyde solution for histopathological examination. Tissues were stained immunohistochemically with APO 2.7 and positive expression apoptotic cells were counted using a Clemex Vision Lite 3.5 vision analysis system.
There were 2-3 apoptotic cells in the control group (group 1) and this number increased to 8-11 in the haemorrhagic shock group (group 2) (p<0.05). Secondary or more serious injury occurs during ischemic reperfusion injury. The number of apoptotic cells increased to 11-14 at the 1st hour (group 3) and it was significant as compared to group 2 (p<0.05). The number of apoptotic cells significantly increased to 15-17 by the 3rd hour (group 4) as compared to group 3 (p<0.05). While there was no additional increase by the end of the 6th hour (group 5) as compared to group 4, the number of apoptotic cells significantly increased to 18-24 by the end of 24th hour (group 6) as compared to group 5 (p<0.05).
The majority of injuries to the brain following haemorrhagic shock occur during ischemic reperfusion. We observed that apoptosis increases step by step on the 1st, 3rd and 24th hours after ischemic reperfusion injury.
细胞凋亡是一种程序性细胞死亡过程，在一些正常和病理状况中发挥作用。在本研究中，我们在大鼠模型中探究了出血性休克后大脑缺血再灌注损伤期间的细胞凋亡情况。
将36只成年Sprague-Dawley大鼠分为六组：对照组、出血性休克组（HS）、缺血再灌注组（IR）、缺血再灌注1小时组、缺血再灌注3小时组、缺血再灌注6小时组和缺血再灌注24小时组。实验结束后通过心内采血处死大鼠。组织用10%中性缓冲甲醛溶液固定以进行组织病理学检查。组织用APO 2.7进行免疫组织化学染色，并用Clemex Vision Lite 3.5视觉分析系统对阳性表达的凋亡细胞进行计数。
对照组（第1组）有2 - 3个凋亡细胞，出血性休克组（第2组）该数量增加至8 - 11个（p<0.05）。缺血再灌注损伤期间会发生继发性或更严重的损伤。凋亡细胞数量在第1小时增加至11 - 14个（第3组），与第2组相比具有显著性差异（p<0.05）。与第3组相比，到第3小时凋亡细胞数量显著增加至15 - 17个（第4组）（p<0.05）。与第4组相比，第6小时末（第5组）凋亡细胞数量没有进一步增加，但与第5组相比，到第24小时末凋亡细胞数量显著增加至18 - 24个（第6组）（p<0.05）。
出血性休克后大脑的大多数损伤发生在缺血再灌注期间。我们观察到缺血再灌注损伤后第1、3和24小时细胞凋亡逐步增加。
