2018
DOI: 10.1007/s12035-018-1400-6
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Anti-vasospastic Effects of Epidermal Growth Factor Receptor Inhibitors After Subarachnoid Hemorrhage in Mice

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Cited by 17 publications
(19 citation statements)
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“…Delayed cerebral ischemia may be caused by cerebral vasospasm, cortical spreading depolarization, and microcirculatory dysfunction [12], which may occur secondary to EBI [13]. Although cerebral vasospasm remains an important cause of delayed cerebral ischemia [14], microcirculatory disturbance and cortical spreading depolarization may be more important than cerebral vasospasm as to the impact on functional outcomes especially in poor-grade SAH patients [15]. Thus, many basic researchers have worked hard to overcome EBI, which is believed eventually to improve outcomes of poor-grade SAH patients.…”
mentioning
confidence: 99%
“…Delayed cerebral ischemia may be caused by cerebral vasospasm, cortical spreading depolarization, and microcirculatory dysfunction [12], which may occur secondary to EBI [13]. Although cerebral vasospasm remains an important cause of delayed cerebral ischemia [14], microcirculatory disturbance and cortical spreading depolarization may be more important than cerebral vasospasm as to the impact on functional outcomes especially in poor-grade SAH patients [15]. Thus, many basic researchers have worked hard to overcome EBI, which is believed eventually to improve outcomes of poor-grade SAH patients.…”
mentioning
confidence: 99%
“…Approximately 10% to 16% of patients die before hospital admission, and around 25% patients remain dependent on assistance [8]. Clinical symptoms of SAH include varying degrees of neurological disorders, from headache and aphasia to hemiplegia or coma [3,4]. The most common clinical symptom in our study was headaches ( Table 2).…”
Section: Discussionmentioning
confidence: 78%
“…Despite improvements in diagnostic and therapeutic techniques, SAH has a high morbidity and mortality rate. Moreover, only 25% of patients are able to live without assistance [1,3,4].…”
Section: Introductionmentioning
confidence: 99%
“…VEGF receptor2 (VEGFR-2), which is a major receptor of VEGF, was reported to be activated after experimental SAH and, VEGFR2 blockage suppresses post-SAH bloodbrain barrier (BBB) damage [12]. VEGFR involvement in the pathophysiology of SAH in cerebral arteries was also reported [13]. To our best knowledge there is no previous study evaluating the impact of anti_VEGF treatment effects after SAH.…”
Section: Discussionmentioning
confidence: 99%