4.5 Review

Central sympathetic nerve activation in subarachnoid hemorrhage

Journal

JOURNAL OF NEUROCHEMISTRY
Volume 160, Issue 1, Pages 34-50

Publisher

WILEY
DOI: 10.1111/jnc.15511

Keywords

catecholamine surge; central sympathetic nerve; extracerebral organ injury; hypothalamus; renin-angiotensin system; subarachnoid hemorrhage

Funding

  1. JSPS KAKENHI [19K09459]
  2. Grants-in-Aid for Scientific Research [19K09459] Funding Source: KAKEN

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SAH is a life-threatening condition with complications related to the sympathetic nerve system, leading to disruptions in brain homeostasis. Further research is needed to understand the specific roles of the sympathetic nerve system in brain injuries associated with SAH.
Subarachnoid hemorrhage (SAH) is a life-threatening condition, and although its two main complications-cerebral vasospasm (CVS)/delayed cerebral ischemia (DCI) and early brain injury (EBI)-have been widely studied, prognosis has not improved over time. The sympathetic nerve (SN) system is important for the regulation of cardiovascular function and is closely associated with cerebral vessels and the regulation of cerebral blood flow and cerebrovascular function; thus, excessive SN activation leads to a rapid breakdown of homeostasis in the brain. In the hyperacute phase, patients with SAH can experience possibly lethal conditions that are thought to be associated with SN activation (catecholamine surge)-related arrhythmia, neurogenic pulmonary edema, and irreversible injury to the hypothalamus and brainstem. Although the role of the SN system in SAH has long been investigated and considerable evidence has been collected, the exact pathophysiology remains undetermined, mainly because the relationships between the SN system and SAH are complicated, and many SN-modulating factors are involved. Thus, research concerning these relationships needs to explore novel findings that correlate with the relevant concepts based on past reliable evidence. Here, we explore the role of the central SN (CSN) system in SAH pathophysiology and provide a comprehensive review of the functional CSN network; brain injury in hyperacute phase involving the CSN system; pathophysiological overlap between the CSN system and the two major SAH complications, CVS/DCI and EBI; CSN-modulating factors; and SAH-related extracerebral organ injury. Further studies are warranted to determine the specific roles of the CSN system in the brain injuries associated with SAH.

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