Abstract
Static cerebral blood flow (CBF) autoregulation maintains a constant CBF despite changes in cerebral perfusion pressure (CPP) within certain limits; this is achieved through adaptive responses in the cerebrovascular resistance, i.e. arteriolar vasoconstriction and vasodilation. This system may protect the brain from hyper- and hypoperfusion upon CPP challenges. CBF autoregulation appears to be mediated through myogenic and metabolic feedback systems, which may involve the vasoconstrictor 20-hydroxyeicosatetraenoic acid as well as an oxygen-sensing mechanism that may involve nitric oxide signalling. Static CBF autoregulation is modulated or impaired in various pathological conditions. In chronic arterial hypertension, both the lower and upper limit of CBF autoregulation are shifted towards higher CPPs; however, CBF autoregulation may be readapted to normal by antihypertensive therapy. Furthermore, CBF autoregulation is impaired in a wide range of clinical conditions, including cerebral ischaemia, traumatic brain injury, intracranial space-occupying processes, subarachnoid haemorrhage, acute bacterial meningitis, fulminant hepatic failure and diabetes. In some of these conditions, CBF autoregulation may be restored by means of hyperventilation and/or induced hypothermia. At present, the clinical impact of CBF autoregulation impairment and of treatment strategies that aim to restore CBF autoregulation remains unclear.
Keywords: 20-hydroxyeicosatetraenoic acid, antihypertensive therapy, cerebral blood flow autoregulation, chronic arterial hypertension, nitric oxide
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