Drug-Induced Hypothermia as Beneficial Treatment before and after Cerebral Ischemia

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Standard

Drug-Induced Hypothermia as Beneficial Treatment before and after Cerebral Ischemia. / Johansen, Flemming F; Hasseldam, Henrik; Rasmussen, Rune Skovgaard; Bisgård, Anne Sofie; Bonfils, Peter Kramshøj; Poulsen, Steen Seier; Hansen-Schwartz, Jacob.

I: Pathobiology, Bind 81, Nr. 1, 2014, s. 42-52.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningfagfællebedømt

Harvard

Johansen, FF, Hasseldam, H, Rasmussen, RS, Bisgård, AS, Bonfils, PK, Poulsen, SS & Hansen-Schwartz, J 2014, 'Drug-Induced Hypothermia as Beneficial Treatment before and after Cerebral Ischemia', Pathobiology, bind 81, nr. 1, s. 42-52. https://doi.org/10.1159/000352026

APA

Johansen, F. F., Hasseldam, H., Rasmussen, R. S., Bisgård, A. S., Bonfils, P. K., Poulsen, S. S., & Hansen-Schwartz, J. (2014). Drug-Induced Hypothermia as Beneficial Treatment before and after Cerebral Ischemia. Pathobiology, 81(1), 42-52. https://doi.org/10.1159/000352026

Vancouver

Johansen FF, Hasseldam H, Rasmussen RS, Bisgård AS, Bonfils PK, Poulsen SS o.a. Drug-Induced Hypothermia as Beneficial Treatment before and after Cerebral Ischemia. Pathobiology. 2014;81(1):42-52. https://doi.org/10.1159/000352026

Author

Johansen, Flemming F ; Hasseldam, Henrik ; Rasmussen, Rune Skovgaard ; Bisgård, Anne Sofie ; Bonfils, Peter Kramshøj ; Poulsen, Steen Seier ; Hansen-Schwartz, Jacob. / Drug-Induced Hypothermia as Beneficial Treatment before and after Cerebral Ischemia. I: Pathobiology. 2014 ; Bind 81, Nr. 1. s. 42-52.

Bibtex

@article{0161ff1e753c4d33b9e0120b92f9c2c3,
title = "Drug-Induced Hypothermia as Beneficial Treatment before and after Cerebral Ischemia",
abstract = "Objectives: Hypothermia is still unproven as beneficial treatment in human stroke, although in animal models, conditioning the brain with hypothermia has induced tolerance to insults. Here, we delineate the feasibility of drug-induced mild hypothermia in reducing ischemic brain damage when conditioning before (preconditioning) and after (postconditioning) experimental stroke. Methods: Hypothermia was induced in rats with a bolus of 6 mg/kg talipexole followed by 20 h continuous talipexole infusion of 6 mg/kg in total. Controls received similar treatment with saline. The core body temperature was continuously monitored. In preconditioning, hypothermia was terminated before either reversible occlusion of the middle cerebral artery (MCAO) for 60 min or global ischemia for 10 min with 2-vessel occlusion and hypotension. In postconditioning, rats experienced 60 min of MCAO before hypothermia was induced either immediately or with 3 h delay. Rats survived ischemia for 2, 7 or 90 days. Infarct volumes were quantified by stereology. Additional experiments of methodological relevance were included in the study. Results: Talipexole induced mild hypothermia (35.1 ± 1.1 to 36.0 ± 0.5°C) for ",
author = "Johansen, {Flemming F} and Henrik Hasseldam and Rasmussen, {Rune Skovgaard} and Bisg{\aa}rd, {Anne Sofie} and Bonfils, {Peter Kramsh{\o}j} and Poulsen, {Steen Seier} and Jacob Hansen-Schwartz",
note = "Copyright {\textcopyright} 2013 S. Karger AG, Basel.",
year = "2014",
doi = "10.1159/000352026",
language = "English",
volume = "81",
pages = "42--52",
journal = "Pathobiology",
issn = "1015-2008",
publisher = "S Karger AG",
number = "1",

}

RIS

TY - JOUR

T1 - Drug-Induced Hypothermia as Beneficial Treatment before and after Cerebral Ischemia

AU - Johansen, Flemming F

AU - Hasseldam, Henrik

AU - Rasmussen, Rune Skovgaard

AU - Bisgård, Anne Sofie

AU - Bonfils, Peter Kramshøj

AU - Poulsen, Steen Seier

AU - Hansen-Schwartz, Jacob

N1 - Copyright © 2013 S. Karger AG, Basel.

PY - 2014

Y1 - 2014

N2 - Objectives: Hypothermia is still unproven as beneficial treatment in human stroke, although in animal models, conditioning the brain with hypothermia has induced tolerance to insults. Here, we delineate the feasibility of drug-induced mild hypothermia in reducing ischemic brain damage when conditioning before (preconditioning) and after (postconditioning) experimental stroke. Methods: Hypothermia was induced in rats with a bolus of 6 mg/kg talipexole followed by 20 h continuous talipexole infusion of 6 mg/kg in total. Controls received similar treatment with saline. The core body temperature was continuously monitored. In preconditioning, hypothermia was terminated before either reversible occlusion of the middle cerebral artery (MCAO) for 60 min or global ischemia for 10 min with 2-vessel occlusion and hypotension. In postconditioning, rats experienced 60 min of MCAO before hypothermia was induced either immediately or with 3 h delay. Rats survived ischemia for 2, 7 or 90 days. Infarct volumes were quantified by stereology. Additional experiments of methodological relevance were included in the study. Results: Talipexole induced mild hypothermia (35.1 ± 1.1 to 36.0 ± 0.5°C) for

AB - Objectives: Hypothermia is still unproven as beneficial treatment in human stroke, although in animal models, conditioning the brain with hypothermia has induced tolerance to insults. Here, we delineate the feasibility of drug-induced mild hypothermia in reducing ischemic brain damage when conditioning before (preconditioning) and after (postconditioning) experimental stroke. Methods: Hypothermia was induced in rats with a bolus of 6 mg/kg talipexole followed by 20 h continuous talipexole infusion of 6 mg/kg in total. Controls received similar treatment with saline. The core body temperature was continuously monitored. In preconditioning, hypothermia was terminated before either reversible occlusion of the middle cerebral artery (MCAO) for 60 min or global ischemia for 10 min with 2-vessel occlusion and hypotension. In postconditioning, rats experienced 60 min of MCAO before hypothermia was induced either immediately or with 3 h delay. Rats survived ischemia for 2, 7 or 90 days. Infarct volumes were quantified by stereology. Additional experiments of methodological relevance were included in the study. Results: Talipexole induced mild hypothermia (35.1 ± 1.1 to 36.0 ± 0.5°C) for

U2 - 10.1159/000352026

DO - 10.1159/000352026

M3 - Journal article

C2 - 23989388

VL - 81

SP - 42

EP - 52

JO - Pathobiology

JF - Pathobiology

SN - 1015-2008

IS - 1

ER -

ID: 57755122