BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.
BACKGROUND: 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. METHODS: 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. RESULTS: 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). CONCLUSION: 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.