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  • Koskinen, Lars-Owe D.,Professor,1955-Department of Physiology and Medical Biophysics, Biomedical Centre, University of Uppsala, Uppsala, Sweden. (author)

Effects of raised intracranial pressure on regional cerebral blood flow : a comparison of effects of naloxone and TRH on the microcirculation in partial cerebral ischaemia.

  • Article/chapterEnglish1985

Publisher, publication year, extent ...

  • 2012-07-19
  • Wiley,1985
  • printrdacarrier

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  • LIBRIS-ID:oai:DiVA.org:umu-167517
  • https://urn.kb.se/resolve?urn=urn:nbn:se:umu:diva-167517URI
  • https://doi.org/10.1111/j.1476-5381.1985.tb08886.xDOI

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  • Language:English
  • Summary in:English

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  • Subject category:ref swepub-contenttype
  • Subject category:art swepub-publicationtype

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  • The effects on regional cerebral blood flow (rCBF) of raised intracranial pressure (ICP) and of naloxone and thyrotropin releasing hormone (TRH) during this condition were studied in anaesthetized rabbits. The ICP was elevated until a central ischaemic response was observed. The regional blood flow was determined with the microsphere technique before and during elevation of the ICP (ICPe) and after drug treatment. Total CBF was reduced by about 70% during ICPe while the uveal blood flow increased slightly and some other peripheral tissue blood flows remained unaffected. The administration of TRH caused an increase in mean arterial blood pressure (MAP) from 11.9 +/- 0.6 to 14.6 +/- 0.7 kPa and a normalization of the rCBF. In some peripheral tissues, e.g. gastric mucosa and spleen, TRH reduced the blood flow by 53% and 76%, respectively. In blood pressure stabilized animals no effect on rCBF was seen after TRH. Naloxone had no consistent effect on MAP or local blood flow. It was concluded that in the range of cerebral perfusion pressure studied there was a passive relationship between cerebral blood flow and perfusion pressure. The lack of effect of naloxone and the marked effect of TRH during cerebral ischaemia are consistent with a mechanism of action of TRH not related to a 'physiological' antagonism of opioids.

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  • Department of Physiology and Medical Biophysics, Biomedical Centre, University of Uppsala, Uppsala, Sweden. (creator_code:org_t)

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  • In:British Journal of Pharmacology: Wiley85:2, s. 489-4970007-11881476-5381

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