Endothelin-1 and cerebral blood flow in a porcine model

Dirk Henze, Matthias Menzel, Jens Soukup, Alexander Scharf, Carsten Holz, Norbert Németh, Frank Hanisch, Tobias Clausen

Research output: Contribution to journalArticle

3 Citations (Scopus)

Abstract

The purpose of the study was to investigate whether provoked changes of cerebral perfusion pressure and arterial carbon dioxide tension are able to influence the cerebral metabolism of endothelin-1 (ET-1) in a porcine model. Brain tissue oxygen tension, regional cerebral blood flow and mean arterial blood pressure were monitored in 10 healthy pigs during induced hyperventilation (HV), hypertension (HrT) and hypotension (HoT). ET-1 was determined in the arterial and cerebrovenous blood. Microdialysis samples (lactate, glucose and pyruvate) were taken from brain and subcutaneous tissue. A significant decrease (p < 0.05) of the arterial ET-1 (1.46 ± 0.33 fmol/mL) compared to the baseline (2.18 ± 0.36 fmol/mL) was observed after the HoT-period. We detected a positive correlation between cerebrovenous ET-1 and extracellular cerebral glucose (0.68; p < 0.05) after the baseline as well as a negative correlation of -0.81 (p < 0.005) between the cerebrovenous ET-1 level and the extracellular cerebral lactate after the HoT-period. These data imply that with increasingly pathological changes of the cerebral metabolism endothelin becomes progressively more important in the regulation of cerebral vascular tone.

Original languageEnglish
Pages (from-to)650-657
Number of pages8
JournalJournal of Clinical Neuroscience
Volume14
Issue number7
DOIs
Publication statusPublished - Jul 1 2007

Keywords

  • Brain tissue oxygen tension
  • Cerebral blood flow
  • Cerebral metabolism
  • Endothelin
  • Porcine model

ASJC Scopus subject areas

  • Surgery
  • Neurology
  • Clinical Neurology
  • Physiology (medical)

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  • Cite this

    Henze, D., Menzel, M., Soukup, J., Scharf, A., Holz, C., Németh, N., Hanisch, F., & Clausen, T. (2007). Endothelin-1 and cerebral blood flow in a porcine model. Journal of Clinical Neuroscience, 14(7), 650-657. https://doi.org/10.1016/j.jocn.2006.05.017