Abstract
Background: Maintenance of brain circulation during shock is sufficient to prevent subcortical injury but the cerebral cortex is not spared. This suggests area-specific regulation of cerebral blood flow (CBF) during hemorrhage. Methods: Cortical and subcortical CBF were continuously measured during blood loss (≤50%) and subsequent reperfusion using laser Doppler flowmetry. Blood gases, mean arterial blood pressure (MABP), heart rate and renal blood flow were also monitored. Urapidil was used for α1A-adrenergic receptor blockade in dosages, which did not modify the MABP-response to blood loss. Western blot and quantitative reverse transcription polymerase chain reactions were used to determine adrenergic receptor expression in brain arterioles. Results: During hypovolemia subcortical CBF was maintained at 81 ± 6% of baseline, whereas cortical CBF decreased to 40 ± 4% (p < 0.001). Reperfusion led to peak CBFs of about 70% above baseline in both brain regions. α1A-Adrenergic blockade massively reduced subcortical CBF during hemorrhage and reperfusion, and prevented hyperperfusion during reperfusion in the cortex. α1A-mRNA expression was significantly higher in the cortex, whereas α1D-mRNA expression was higher in the subcortex (p < 0.001). Conclusions: α1-Adrenergic receptors are critical for perfusion redistribution: activity of the α1A-receptor subtype is a prerequisite for redistribution of CBF, whereas the α1D-receptor subtype may determine the magnitude of redistribution responses.
Highlights
Severe bleeding is a common cause of disability following traumatic ruptures of large vessels and parenchymal organs, gastrointestinal bleeding or placenta abruption [1,2,3,4,5]
We further considered the possibility that regional differences in α1-adrenergic receptor densities exist and that these differences enable region-specific maintenance of cerebral perfusion during severe hemorrhage
It is known that the degree of the decrease of cerebral perfusion is correlated to the severity of brain damage [3]
Summary
Severe bleeding (hemorrhage) is a common cause of disability following traumatic ruptures of large vessels and parenchymal organs, gastrointestinal bleeding or placenta abruption [1,2,3,4,5]. We tested the hypothesis that the effectiveness of cerebral redistribution mechanisms under clinically relevant conditions (hemorrhagic shock) is inferior in the phylogenetic younger cerebral cortex than in the phylogenetically older subcortex, which contains vital regions such as the respiration and circulation control centers. The plausibility of this hypothesis is supported by some evidence for differences in cerebral blood supply in different brain regions [13]. Maintenance of brain circulation during shock is sufficient to prevent subcortical injury but the cerebral cortex is not spared This suggests area-specific regulation of cerebral blood flow (CBF) during hemorrhage. Conclusions: α1-Adrenergic receptors are critical for perfusion redistribution: activity of the α1A-receptor subtype is a prerequisite for redistribution of CBF, whereas the α1D-receptor subtype may determine the magnitude of redistribution responses
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