Molecular mechanisms of early brain injury after subarachnoid hemorrhage.
OBJECTIVE
Increasing body of experimental and clinical data indicates that early brain injury after initial bleeding largely contributes to unfavorable outcome after subarachnoid hemorrhage (SAH). This review presents molecular mechanisms underlying brain injury at its early stages after SAH.


METHODS
PubMed was searched using term 'subarachnoid hemorrhage' and key words referring to molecular and cellular pathomechanisms of SAH-induced early brain injury.


RESULTS
The authors reviewed intracranial phenomena and molecular agents that contribute to the early development of pathological sequelae of SAH in cerebral and vascular tissues, including cerebral ischemia and its interactions with injurious blood components, blood-brain barrier disruption, brain edema and apoptosis.


CONCLUSIONS
It is believed that detailed knowledge of molecular signaling pathways after SAH will serve to improve therapeutic interventions. The most promising approach is the protection of neurovascular unit including anti-apoptosis therapy.
Ostrowski
Robert P
RP
Department of Physiology, Loma Linda University, CA 92354, USA.
Colohan
Austin R
AR
Zhang
John H
JH
D000818:Animals; D017209:Apoptosis / Q000502:physiology; D001929:Brain Edema / Q000209:etiology / Q000473:pathology; D001930:Brain Injuries / Q000150:complications / Q000209:etiology* / Q000473:pathology / Q000503:physiopathology*; D002545:Brain Ischemia / Q000209:etiology / Q000473:pathology; D002560:Cerebrovascular Circulation / Q000502:physiology; D006801:Humans; D007249:Inflammation; D008954:Models, Biological; D039781:PubMed / Q000706:statistics & numerical data; D015398:Signal Transduction / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications* / Q000378:metabolism*