Apoptotic mechanisms for neuronal cells in early brain injury after subarachnoid hemorrhage.
OBJECTIVE
The major causes of death and disability in subarachnoid hemorrhage (SAH) may be early brain injury (EBI) and cerebral vasospasm. Although cerebral vasospasm has been studied and treated by a lot of drugs, the outcome is not improved even if vasospasm is reversed. Based on these data, EBI is considered a primary target for future research, and apoptosis may be involved in EBI after experimental SAH.


METHODS
We reviewed the published literature about the relationship between SAH induced EBI and apoptosis in PubMed.


RESULTS
Most available information can be obtained from the endovascular filament perforation animal model. After onset of SAH, intracranial pressure is increased and then cerebral blood flow is reduced. Many factors are involved in the mechanism of apoptotic cell death in EBI after SAH. In the neuronal cells, both intrinsic and extrinsic pathways of apoptosis can occur. Some antiapoptotic drugs were studied and demonstrated a protective effect against EBI after SAH. However, apoptosis in EBI after SAH has been little studied and further studies will provide us more beneficial findings.


CONCLUSIONS
The study of apoptosis in EBI after experimental SAH may give us new therapies for SAH.
Department of Physiology, Loma Linda University School of Medicine, Loma Linda, CA 92354, USA.
Yu
Y
Hasegawa
Hidenori
H
Suzuki
Takumi
T
Sozen
Orhan
O
Altay
John H
JH
Zhang
D000818:Animals; D017209:Apoptosis / Q000502:physiology*; D001930:Brain Injuries / Q000209:etiology* / Q000401:mortality / Q000473:pathology*; D004249:DNA Damage / Q000502:physiology; D004195:Disease Models, Animal; D006801:Humans; D008954:Models, Biological; D009474:Neurons / Q000502:physiology*; D018384:Oxidative Stress / Q000502:physiology; D039781:PubMed / Q000706:statistics & numerical data; D015398:Signal Transduction / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications*