Publication: Cerebrovascular pathophysiology of delayed cerebral ischemia after aneurysmal subarachnoid hemorrhage
Authors
Suzuki, Hidenori ; Kanamaru, Hideki ; Kawakita, Fumihiro ; Asada, Reona ; Fujimoto, Masashi ; Shiba, Masato
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-253
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info:eu-repo/semantics/article
Description
Abstract
Aneurysmal subarachnoid hemorrhage
(SAH) remains a serious cerebrovascular disease. Even
if SAH patients survive the initial insults, delayed
cerebral ischemia (DCI) may occur at 4 days or later
post-SAH. DCI is characteristics of SAH, and is
considered to develop by blood breakdown products and
inflammatory reactions, or secondary to early brain
injury, acute pathophysiological events that occur in the
brain within the first 72 hours of aneurysmal SAH. The
pathology underlying DCI may involve large artery
vasospasm and/or microcirculatory disturbances by
microvasospasm, microthrombosis, dysfunction of
venous outflow and compression of microvasculature by
vasogenic or cytotoxic tissue edema. Recent clinical
evidence has shown that large artery vasospasm is not
the only cause of DCI, and that both large artery
vasospasm-dependent and -independent cerebral
infarction causes poor outcome. Animal studies suggest
that mechanisms of vasospasm may differ between large
artery and arterioles or capillaries, and that many kinds
of cells in the vascular wall and brain parenchyma may
be involved in the pathogenesis of microcirculatory
disturbances. The impairment of the paravascular and
glymphatic systems also may play important roles in the
development of DCI. As pathological mediators for DCI,
glutamate and several matricellular proteins have been
investigated in addition to inflammatory molecules.
Glutamate is involved in excitotoxicity contributing to
cortical spreading ischemia and epileptic activity-related
events. Microvascular dysfunction is an attractive
mechanism to explain the cause of poor outcomes
independently of large cerebral artery vasospasm, but
needs more studies to clarify the pathophysiologies or
mechanisms and to develop a novel therapeutic strategy.
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Citation
Histology and Histopathology Vol. 36, nĀŗ2 (2021)
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