Redistribution of Cerebral Blood Flow during Severe Hypovolemia and Reperfusion in a Sheep Model: Critical Role of α1-Adrenergic Signaling.

Autor: Schiffner R; Orthopedic Department, Campus Eisenberg, Jena University Hospital-Friedrich Schiller University, 07607 Eisenberg, Germany. rene.schiffner@med.uni-jena.de.; Department of Neurology; Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. rene.schiffner@med.uni-jena.de., Bischoff SJ; Institute for Laboratory Animal Sciences and Welfare, Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. Sabine.Bischoff@med.uni-jena.de., Lehmann T; Institute of Medical Statistics, Computer Sciences and Documentation Science, Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. thomas.lehmann@med.uni-jena.de., Rakers F; Department of Neurology; Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. Florian.Rakers@med.uni-jena.de., Rupprecht S; Department of Neurology; Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. Sven.Rupprecht@med.uni-jena.de., Reiche J; Institute for Biochemistry II, Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. Juliane.Reiche@med.uni-jena.de., Matziolis G; Orthopedic Department, Campus Eisenberg, Jena University Hospital-Friedrich Schiller University, 07607 Eisenberg, Germany. G.Matziolis@krankenhaus-eisenberg.de., Schubert H; Institute for Laboratory Animal Sciences and Welfare, Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. harald.schubert@outlook.de., Schwab M; Department of Neurology; Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. Matthias.Schwab@med.uni-jena.de., Huber O; Institute for Biochemistry II, Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. Otmar.Huber@med.uni-jena.de., Schmidt M; Institute for Biochemistry II, Jena University Hospital-Friedrich Schiller University, 07743 Jena, Germany. Martin.Schmidt@med.uni-jena.de.
Jazyk: angličtina
Zdroj: International journal of molecular sciences [Int J Mol Sci] 2017 May 11; Vol. 18 (5). Date of Electronic Publication: 2017 May 11.
DOI: 10.3390/ijms18051031
Abstrakt: 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.
Databáze: MEDLINE
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