Cerebral microvasculature is an early target of subarachnoid hemorrhage.
Most subarachnoid hemorrhage (SAH) patients exhibit clinical signs of cerebral ischemia at admission but no angiographic vasospasm. Consequently, the source of early cerebral ischemia is not understood. Parenchymal microvessels may contribute to early cerebral ischemia, but the low resolution of current imaging has prevented their analysis in SAH patients. Animal studies demonstrated that early after SAH structure and function of parenchymal vessels are compromised to the level that may very well contribute to early ischemia. We review these studies.
Department of Neurosurgery and Neurosciences, Mount Sinai School of Medicine, New York, NY 10029, USA. fatima.sehba@mssm.edu
Fatima A
FA
Sehba
Victor
V
Friedrich
D000818:Animals; D002540:Cerebral Cortex / Q000473:pathology*; D004195:Disease Models, Animal; D004660:Encephalitis / Q000209:etiology / Q000473:pathology; D006801:Humans; D055806:Microvessels / Q000503:physiopathology* / Q000648:ultrastructure; D009422:Nervous System Diseases / Q000209:etiology; D009569:Nitric Oxide / Q000378:metabolism; D019001:Nitric Oxide Synthase / Q000378:metabolism; D018384:Oxidative Stress / Q000502:physiology; D015398:Signal Transduction / Q000502:physiology; D013345:Subarachnoid Hemorrhage / Q000150:complications / Q000473:pathology*
D009569:Nitric Oxide; D019001:Nitric Oxide Synthase