Inflammation and cerebral vasospasm after subarachnoid hemorrhage.
Morbidity and mortality of patients with aneurysmal subarachnoid hemorrhage (aSAH) is significantly related to the development of chronic cerebral vasospasm. Despite extensive clinical and experimental research, the pathophysiology of the events that result in delayed arterial spasm is not fully understood. A review of the published literature on cerebral vasospasm that included but was not limited to all PubMed citations from 1951 to the present was performed. The findings suggest that leukocyte-endothelial cell interactions play a significant role in the pathophysiology of cerebral vasospasm and explain the clinical variability and time course of the disease. Experimental therapeutic targeting of the inflammatory response when timed correctly can prevent vasospasm, and supplementation of endothelial relaxation by nitric oxide-related therapies and other approaches could result in reversal of the arterial narrowing and improved outcomes in patients with aSAH.
Pradilla
Gustavo
G
Division of Cerebrovascular Neurosurgery, Department of Neurosurgery, The Johns Hopkins University School of Medicine, Meyer Building 8-181, 600 North Wolfe Street, Baltimore, MD 21287, USA.
Chaichana
Kaisorn L
KL
Hoang
Stanley
S
Huang
Judy
J
Tamargo
Rafael J
RJ
D000893:Anti-Inflammatory Agents / Q000494:pharmacology / Q000627:therapeutic use; D002536:Cerebral Arteries / Q000473:pathology / Q000503:physiopathology*; D042783:Endothelial Cells / Q000187:drug effects / Q000502:physiology; D006801:Humans; D007962:Leukocytes / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications*; D020293:Vasculitis, Central Nervous System / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*; D014665:Vasodilator Agents / Q000494:pharmacology / Q000627:therapeutic use; D020301:Vasospasm, Intracranial / Q000188:drug therapy / Q000209:etiology / Q000503:physiopathology*
D000893:Anti-Inflammatory Agents; D014665:Vasodilator Agents