TY - GEN
T1 - Advances in Experimental Subarachnoid Hemorrhage
AU - Sozen, Takumi
AU - Tsuchiyama, Reiko
AU - Hasegawa, Yu
AU - Suzuki, Hidenori
AU - Jadhav, Vikram
AU - Nishizawa, Shigeru
AU - Zhang, John H.
N1 - Subarachnoid hemorrhage (SAH) remains to be a devastating disease with high mortality and morbidity. Two major areas are becoming the focus of the research interest of SAH: these are cerebral vasospas
PY - 2011
Y1 - 2011
N2 - Subarachnoid hemorrhage (SAH) remains to be a devastating disease with high mortality and morbidity. Two major areas are becoming the focus of the research interest of SAH: these are cerebral vasospasm (CVS) and early brain injury (EBI). This mini review will provide a broad summary of the major advances in experimental SAH during the last 3 years. Treatments interfering with nitric oxide (NO)- or endothelin-pathways continue to show antispasmotic effects in experimental SAH. HIF 1 may play both a detrimental and beneficial role in the setting of SAH, depending on its activation stage. Inflammation and oxidative stress contribute to the pathophysiology of both CVS and EBI. Apoptosis, a major component of EBI after SAH, also underlie the etiology of CVS. Since we recognize now that CVS and EBI are the two major contributors to the significant mortality and morbidity associated with SAH, ongoing research will continue to elucidate the underlying pathophysiological pathways and treatment strategies targeting both CVS and EBI may be more successful and improve outcome of patients with SAH. © 2011 Springer-Verlag/Wien.
AB - Subarachnoid hemorrhage (SAH) remains to be a devastating disease with high mortality and morbidity. Two major areas are becoming the focus of the research interest of SAH: these are cerebral vasospasm (CVS) and early brain injury (EBI). This mini review will provide a broad summary of the major advances in experimental SAH during the last 3 years. Treatments interfering with nitric oxide (NO)- or endothelin-pathways continue to show antispasmotic effects in experimental SAH. HIF 1 may play both a detrimental and beneficial role in the setting of SAH, depending on its activation stage. Inflammation and oxidative stress contribute to the pathophysiology of both CVS and EBI. Apoptosis, a major component of EBI after SAH, also underlie the etiology of CVS. Since we recognize now that CVS and EBI are the two major contributors to the significant mortality and morbidity associated with SAH, ongoing research will continue to elucidate the underlying pathophysiological pathways and treatment strategies targeting both CVS and EBI may be more successful and improve outcome of patients with SAH. © 2011 Springer-Verlag/Wien.
KW - Cerebral vasospasm (CVS)
KW - Early brain injury (EBI)
KW - Subarachnoid hemorrhage (SAH)
KW - Endothelins/metabolism
KW - Subarachnoid Hemorrhage/complications
KW - Animals
KW - Humans
KW - Ischemia/etiology
KW - Nitric Oxide/metabolism
KW - Vasospasm, Intracranial/etiology
KW - Disease Models, Animal
KW - Signal Transduction/physiology
UR - http://europepmc.org/abstract/MED/21116908
U2 - 10.1007/978-3-7091-0353-1_3
DO - 10.1007/978-3-7091-0353-1_3
M3 - Conference contribution
C2 - 21116908
SN - 9783709103524
VL - 110
T3 - Acta Neurochirurgica, Supplementum
SP - 15
EP - 21
BT - Early Brain Injury or Cerebral Vasospasm
PB - Springer-Verlag Wien
ER -