Abstract
While the cerebral autoregulation sufficiently protects subcortical brain regions during hypoxia or asphyxia, the cerebral cortex is not as adequately protected, which suggests that regulation of the cerebral blood flow (CBF) is area-specific. Hypoxia was induced by inhalation of 5% oxygen, for reoxygenation 100% oxygen was used. Cortical and subcortical CBF (by laser Doppler flowmetry), blood gases, mean arterial blood pressure (MABP), heart rate and renal blood flow were constantly monitored. Low dosed urapidil was used for α1A-adrenergic receptor blockade. Western blotting was used to determine adrenergic receptor signalling mediators in brain arterioles. During hypoxia cortical CBF decreased to 72 ± 11% (mean reduction 11 ± 3%, p < 0.001) of baseline, whereas subcortical CBF increased to 168±18% (mean increase 43 ± 5%, p < 0.001). Reoxygenation led to peak CBF of 194 ± 27% in the subcortex, and restored cortical CBF. α1A-Adrenergic blockade led to minor changes in cortical CBF, but massively reduced subcortical CBF during hypoxia and reoxygenation–almost aligning CBF in both brain regions. Correlation analyses revealed that α1A-adrenergic blockade renders all CBF-responses pressure-passive during hypoxia and reoxygenation, and confirmed the necessity of α1A-adrenergic signalling for coupling of CBF-responses to oxygen saturation. Expression levels and activation state of key signalling-mediators of α1-receptors (NOSs, CREB, ERK1/2) did not differ between cortex and subcortex. The dichotomy between subcortical and cortical CBF during hypoxia and reoxygenation critically depends on α1A-adrenergic receptors, but not on differential expression of signalling-mediators: signalling through the α1A-subtype is a prerequisite for cortical/subcortical redistribution of CBF.
Highlights
Neurological deficits and impairments are in many cases accompanied by a significant decrease in the patients’ quality of life and capability to uphold their former lifestyle, both in regard to private and work-related matters
While the primary treatment for all of the above mentioned emergencies is either reoxygenation or, respectively, reperfusion, cerebral autoregulatory mechanisms are able to protect the brain from both hypoperfusion and ischemia through changes in the cerebral blood flow (CBF) up to a certain point [12, 13] albeit the degree of brain protection by autoregulation depends on the underlying cause of damage
From the results of this study we draw the conclusion that, during states of hypoxia, subcortical brain regions exhibit a superior protection through the cerebral autoregulation as compared to the cerebral cortex, which can be attributed to region-specific regulation of the CBF
Summary
Neurological deficits and impairments are in many cases accompanied by a significant decrease in the patients’ quality of life and capability to uphold their former lifestyle, both in regard to private and work-related matters. The long-term consequences of an ischaemic episode suffered by the brain are mostly determined by the extent of damage sustained by the cerebral cortex [9, 10]. This notion was experimentally confirmed in a sheep model of ischemia, where lesions in the cerebral cortex and striatum were observed earlier than lesions in e.g. the thalamic region [11]. While the primary treatment for all of the above mentioned emergencies is either reoxygenation or, respectively, reperfusion, cerebral autoregulatory mechanisms are able to protect the brain from both hypoperfusion and ischemia through changes in the cerebral blood flow (CBF) up to a certain point [12, 13] albeit the degree of brain protection by autoregulation depends on the underlying cause of damage. While the exact extent of its contribution still remains unknown, a number of studies have identified at least a supporting role in cerebral autoregulatory mechanisms [14,15,16]
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