Infusion of prostacyclin following experimental brain injury in the rat reduces cortical lesion volume

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Bentzer, PeterLund University,Lunds universitet,Anestesiologi och intensivvård,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Anesthesiology and Intensive Care,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine (author)

Infusion of prostacyclin following experimental brain injury in the rat reduces cortical lesion volume

Article/chapterEnglish2001

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Mary Ann Liebert Inc,2001

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LIBRIS-ID:oai:lup.lub.lu.se:74e25e57-4149-4876-affb-3192e03e6f3c
https://lup.lub.lu.se/record/1120013URI
https://doi.org/10.1089/08977150151070919DOI

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Language:English
Summary in:English

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Endothelial-derived prostacyclin is an important regulator of microvascular function, and its main actions are inhibition of platelet/leukocyte aggregation and adhesion, and vasodilation. Disturbances in endothelial integrity following traumatic brain injury (TBI) may result in insufficient prostacyclin production and participate in the pathophysiological sequelae of brain injury. The objective of this study was to evaluate the potential therapeutic effects of a low-dose prostacyclin infusion on cortical lesion volume, CA3 neuron survival and functional outcome following TBI in the rat. Anesthetized animals (sodium pentobarbital, 60 mg/kg, i.p.) were subjected to a lateral fluid percussion brain injury (2.5 atm) or sham injury. Following TBI, animals were randomized to receive a constant infusion of either prostacyclin (1 ng/kg x min(-1) i.v.) or vehicle over 48 h. All sham animals received vehicle (n = 6). Evaluation of neuromotor function, lesion volume, and CA3 neuronal loss was performed blindly. By 7 days postinjury, cortical lesion volume was significantly reduced by 43% in the prostacyclin-treated group as compared to the vehicle treated group (p < 0.01; n = 12 prostacyclin, n = 12 vehicle). No differences were observed in neuromotor function (48 h and 7 days following TBI), or in hippocampal cell loss (7 days following TBI) between the prostacyclin- and vehicle-treated groups. We conclude that prostacyclin in a low dose reduces loss of neocortical neurons following TBI and may be a potential clinical therapeutic agent to reduce neuronal cell death associated with brain trauma.

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Mattiasson, GustavLund University,Lunds universitet,Anestesiologi och intensivvård,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Anesthesiology and Intensive Care,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine,Section IV,Department of Clinical Sciences, Lund(Swepub:lu)efor-gma (author)
McIntosh, T K (author)
Wieloch, TadeuszLund University,Lunds universitet,Sektion IV,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Section IV,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)efor-twi (author)
Grände, Per-OlofLund University,Lunds universitet,Anestesiologi och intensivvård,Sektion II,Institutionen för kliniska vetenskaper, Lund,Medicinska fakulteten,Anesthesiology and Intensive Care,Section II,Department of Clinical Sciences, Lund,Faculty of Medicine(Swepub:lu)mphy-pog (author)
Anestesiologi och intensivvårdSektion II (creator_code:org_t)

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In:Journal of Neurotrauma: Mary Ann Liebert Inc18:3, s. 275-2851557-90420897-7151

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