Abstract
Subarachnoid hemorrhage (SAH) is a subtype of stroke with high mortality and morbidity. Impaired cerebral autoregulation following SAH has been reported owing to effects on sympathetic control, endothelial function, myogenic response, and cerebral metabolism. Impaired cerebral autoregulation is associated with early brain injury, cerebral vasospasm/delayed cerebral ischemia, and SAH prognosis. However, few drugs have been reported to improve cerebral autoregulation after SAH. Melatonin is a powerful antioxidant that is effective (easily crosses the blood brain barrier) and safe (tolerated in large doses without toxicity). Theoretically, melatonin may impact the control mechanisms of cerebral autoregulation via antioxidative effects, protection of endothelial cell integrity, suppression of sympathetic nerve activity, increase in nitric oxide bioavailability, mediation of the myogenic response, and amelioration of hypoxemia. Furthermore, melatonin may have a comprehensive effect on cerebral autoregulation. This review discusses the potential effects of melatonin on cerebral autoregulation following SAH, in terms of the association between pharmacological activities and the mechanisms of cerebral autoregulation.
Highlights
Cerebral autoregulation is defined as the mechanism by which constant cerebral blood flow is maintained, despite changes in arterial blood pressure (Guo et al, 2016)
An increasing number of studies have focused on the relationship between cerebral autoregulation and Subarachnoid hemorrhage (SAH) and have reported that the impairment of cerebral autoregulation is related to poor prognosis after SAH
Otite et al (2014) reported that patients who developed delayed cerebral vasospasm and delayed cerebral ischemia after SAH had worse cerebral autoregulation than did those who did not develop either of the conditions
Summary
Cerebral autoregulation is defined as the mechanism by which constant cerebral blood flow is maintained, despite changes in arterial blood pressure (Guo et al, 2016). Impaired cerebral autoregulation after SAH is possibly caused by oxidative stress, endothelial dysfunction, sympathetic activation, myogenic response disorder, and abnormal cerebral metabolism.
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