The Role of Nitric Oxide and Sympathetic Control in Cerebral Autoregulation in the Setting of Subarachnoid Hemorrhage and Traumatic Brain Injury

Abstract

Cerebral autoregulation is defined as the mechanism by which constant cerebral blood flow is maintained despite changes of arterial blood pressure, and arterial blood pressure represents the principle aspect of cerebral autoregulation. The impairment of cerebral autoregulation is reported to be involved in several diseases. However, the concept, mechanisms, and pathological dysfunction of cerebral autoregulation are beyond full comprehension. Nitric oxide control and sympathetic control are main contributors to cerebral autoregulation. Although impaired cerebral autoregulation after nitric oxide inhibition or sympathetic ganglia blockade is reported, managing the inhibition or blockade can have negative consequences and needs further exploration. Additionally, impaired cerebral autoregulation following subarachnoid hemorrhage and traumatic brain injury has been proven by several descriptive studies, although without corresponding explanations. As the most important mechanisms of cerebral autoregulation, the changes of nitric oxide and sympathetic stimulation play significant roles in these insults. Therefore, the in-depth researches of nitric oxide and sympathetic nerve in cerebral autoregulation may help to develop new therapeutic targets.