Apoptosis and cerebral ischemic reperfusion injury developed after haemorrhagic shock: experimental study

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.

Hemorajik þok sonrasý geliþen serebral iskemi reperfüzyon yaralanmasý ve apoptosis: Deneysel çalýþma

AMAÇ Apoptosis, normal ve patolojik þartlarda gerçekleþen programlanmýþ hücre ölümüdür. Biz bu çalýþmada, hemorajik þoka uðratýlmýþ sýçan modelinde serebral iskemik reperfüzyon hasarýný apoptosis açýsýndan araþtýrdýk. GEREÇ VE YÖNTEM Toplam 36 adet Sprague-Dawley cinsi sýçan; kontrol, hemorajik þok (HS), iskemik reperfüzyon (IR) 1. saat, IR 3. saat, IR 6. saat, IR 24. saat olmak üzere 6 gruba ayrýldý. Sýçanlar, deney çalýþmasý bittikten sonra intrakardiyak yolla kan alýnarak sakrifiye edildiler. Dokular, histopatolojik çalýþma için %10’luk tamponatlý solüsyona alýndý. Dokular APO 2.7 ile immünohistokimyasal olarak boyandý ve pozitif ekspresyon gösteren apoptotik hücreler Clemex Vision Lite 3.5 vision analiz sistemi kullanýlarak sayýldý. BULGULAR Kontrol grubunda (grup 1), 2-3 tane apoptotik hücre vardý ve bu sayý hemorajik þok grubunda (grup 2) 8-11’e çýkýyordu (p<0.05). Iskemik reperfüzyon esnasýnda daha ciddi hasarlar oluþtu. IR’den sonraki 1. saatte (grup 3) apoptotik hücre sayýsý 11-14’dü ve bu sonuç group 2 ile karþýlaþtýrýlýðýnda anlamlýydý (p<0.05). Apoptotik hücre sayýsý 3. saatte (grup 4) 15-17’ye çýktý ve bu sonuç grup 3 ile karþýlaþtýrýldýðýnda anlamlýydý (p<0.05). Apoptotik hücre sayýsýnda IR’den sonra 6.saat sonunda (grup 5) ek bir artýþ meydana gelmezken, 24. saat sonunda (grup 6) 18-24’e çýktý ve bu sonuç grup 5 ile karþýlaþtýrýldýðýnda anlamlýydý (p<0.05). SONUÇ Hemorajik þoku takiben oluþan beyin hasarlarýnýn çoðu iskemik reperfüzyon esnasýnda oluþur. Biz bu çalýþma sonucuna göre, apoptozisin iskemik reperfüzyon sonrasý 1., 3. ve 24. saatlerde adým adým arttýðýný düþünüyoruz.