Abstract
Loss of cerebral autoregulation in normal perfusion pressure breakthrough (NPPB) phenomenon has been reported in other Central Nervous System diseases such as neonatal intraventricular haemorrhage. Several studies have demonstrated that low-dose indomethacin prevents this latter condition. A previous rat model was used to resemble NPPB phenomenon. Study animals were distributed in 4 groups that received 3 doses of indomethacin at different concentrations prior to fistula occlusion 60 days after its creation. Control animals received saline solution. Intracranial pressure (ICP) increased in all groups following fistula creation, whereas mean arterial pressure (MAP) and cerebral perfusion pressure (CPP) decreased as a manifestation of cerebral hypoperfusion and intracranial hypertension. The administration of indomethacin was associated with raised MAP and CPP, as well as decreased ICP. Sodium fluorescein extravasation was slight in study animals when comparing with control ones. Histological analysis evidenced diffuse ischaemic changes with signs of neuronal apoptosis in all brain layers in control animals. These findings were only focal and slight in study animals. The results suggest the usefulness of indomethacin to revert, at least partially, the haemodynamic effects of NPPB phenomenon in this experimental model, as well as to reduce BBB disruption and histological ischemia observed in absence of indomethacin.
Highlights
Loss of cerebral autoregulation in normal perfusion pressure breakthrough (NPPB) phenomenon has been reported in other Central Nervous System diseases such as neonatal intraventricular haemorrhage
The theory was first proposed by Spetzler et al.[1], who considered that the cerebral hemisphere harbouring an arteriovenous malformation (AVM), large-size ones, suffers hypoperfusion and ischemia as a result of a “vascular steal” phenomenon that the AVM exerts on cerebral blood flow (CBF)
Indomethacin administration prior to arteriovenous fistula (AVF) closure was related to a non dose-dependent significant increase in mean arterial pressure (MAP) and cerebral perfusion pressure (CPP)
Summary
Loss of cerebral autoregulation in normal perfusion pressure breakthrough (NPPB) phenomenon has been reported in other Central Nervous System diseases such as neonatal intraventricular haemorrhage. Normal perfusion pressure breakthrough (NPPB) phenomenon is a theoretical explanation that tries to clarify the clinical observation of the development of massive brain swelling and/or diffuse cortical brain haemorrhages following intracranial arteriovenous malformation (AVM) o cclusion[1,2]. The theory was first proposed by Spetzler et al.[1], who considered that the cerebral hemisphere harbouring an AVM, large-size ones, suffers hypoperfusion and ischemia as a result of a “vascular steal” phenomenon that the AVM exerts on cerebral blood flow (CBF) As this phenomenon becomes chronic, the adaptive ability of vascular autoregulation of normal brain tissue surrounding the AVM would be affected and reflected on the permanent arterial dilation in the brain tissue marginal to the AVM, a condition that attempts to increase arterial contribution to counteract vascular steal and, chronic hypoperfusion[1,6,7]. When IVH reaches enough size, a dehiscence in the ventricular ependyma appears and so haemorrhage extends and becomes periventricular–intraventricular[11]
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