Rehabilitation Augments Hematoma Clearance and Attenuates Oxidative Injury and Ion Dyshomeostasis After Brain Hemorrhage

BACKGROUND AND PURPOSE—We assessed the elemental and biochemical effects of rehabilitation after intracerebral hemorrhage, with emphasis on iron-mediated oxidative stress, using a novel multimodal biospectroscopic imaging approach. METHODS—Collagenase-induced striatal hemorrhage was produced in rats...

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Published in:Stroke (1970) 2017-01, Vol.48 (1), p.195-203
Main Authors: Williamson, Michael R, Dietrich, Kristen, Hackett, Mark J, Caine, Sally, Nadeau, Colby A, Aziz, Jasmine R, Nichol, Helen, Paterson, Phyllis G, Colbourne, Frederick
Format: Article
Language:English
Subjects:
Animals
Cerebral Hemorrhage - metabolism
Cerebral Hemorrhage - rehabilitation
Hematoma - metabolism
Hematoma - rehabilitation
Iron - analysis
Iron - metabolism
Male
Oxidative Stress - physiology
Rats
Rats, Sprague-Dawley
Spectrometry, X-Ray Emission - methods
Spectrum Analysis, Raman - methods
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container_end_page 203
container_issue 1
container_start_page 195
container_title Stroke (1970)
container_volume 48
creator Williamson, Michael R
Dietrich, Kristen
Hackett, Mark J
Caine, Sally
Nadeau, Colby A
Aziz, Jasmine R
Nichol, Helen
Paterson, Phyllis G
Colbourne, Frederick
description BACKGROUND AND PURPOSE—We assessed the elemental and biochemical effects of rehabilitation after intracerebral hemorrhage, with emphasis on iron-mediated oxidative stress, using a novel multimodal biospectroscopic imaging approach. METHODS—Collagenase-induced striatal hemorrhage was produced in rats that were randomized to enriched rehabilitation or control intervention starting on day 7. Animals were euthanized on day 14 or 21, a period of ongoing cell death. We used biospectroscopic imaging techniques to precisely determine elemental and molecular changes on day 14. Hemoglobin content was assessed with resonance Raman spectroscopy. X-ray fluorescence imaging mapped iron, chlorine, potassium, calcium, and zinc. Protein aggregation, a marker of oxidative stress, and the distribution of other macromolecules were assessed with Fourier transform infrared imaging. A second study estimated hematoma volume with a spectrophotometric assay at 21 days. RESULTS—In the first experiment, rehabilitation reduced hematoma hemoglobin content (P=0.004) and the amount of peri-hematoma iron (P
doi_str_mv 10.1161/STROKEAHA.116.015404
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METHODS—Collagenase-induced striatal hemorrhage was produced in rats that were randomized to enriched rehabilitation or control intervention starting on day 7. Animals were euthanized on day 14 or 21, a period of ongoing cell death. We used biospectroscopic imaging techniques to precisely determine elemental and molecular changes on day 14. Hemoglobin content was assessed with resonance Raman spectroscopy. X-ray fluorescence imaging mapped iron, chlorine, potassium, calcium, and zinc. Protein aggregation, a marker of oxidative stress, and the distribution of other macromolecules were assessed with Fourier transform infrared imaging. A second study estimated hematoma volume with a spectrophotometric assay at 21 days. RESULTS—In the first experiment, rehabilitation reduced hematoma hemoglobin content (P=0.004) and the amount of peri-hematoma iron (P&lt;0.001). Oxidative damage was highly localized at the hematoma/peri-hematoma border and was decreased by rehabilitation (P=0.004). Lipid content in the peri-hematoma zone was increased by rehabilitation (P=0.016). Rehabilitation reduced the size of calcium deposits (P=0.040) and attenuated persistent dyshomeostasis of Cl (P&lt;0.001) but not K (P=0.060). The second study confirmed that rehabilitation decreased hematoma volume (P=0.024). CONCLUSIONS—Rehabilitation accelerated clearance of toxic blood components and decreased chronic oxidative stress. As well, rehabilitation attenuated persistent ion dyshomeostasis. These novel effects may underlie rehabilitation-induced neuroprotection and improved recovery of function. Pharmacotherapies targeting these mechanisms may further improve outcome.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/STROKEAHA.116.015404</identifier><identifier>PMID: 27899761</identifier><language>eng</language><publisher>United States: American Heart Association, Inc</publisher><subject>Animals ; Cerebral Hemorrhage - metabolism ; Cerebral Hemorrhage - rehabilitation ; Hematoma - metabolism ; Hematoma - rehabilitation ; Iron - analysis ; Iron - metabolism ; Male ; Oxidative Stress - physiology ; Rats ; Rats, Sprague-Dawley ; Spectrometry, X-Ray Emission - methods ; Spectrum Analysis, Raman - methods</subject><ispartof>Stroke (1970), 2017-01, Vol.48 (1), p.195-203</ispartof><rights>2017 American Heart Association, Inc.</rights><rights>2016 American Heart Association, Inc.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4474-101a97f3888521b6d2d8796bb1b4ef888c1129ecc9d2ed979e06d047619b5d883</citedby><cites>FETCH-LOGICAL-c4474-101a97f3888521b6d2d8796bb1b4ef888c1129ecc9d2ed979e06d047619b5d883</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27922,27923</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/27899761$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Williamson, Michael R</creatorcontrib><creatorcontrib>Dietrich, Kristen</creatorcontrib><creatorcontrib>Hackett, Mark J</creatorcontrib><creatorcontrib>Caine, Sally</creatorcontrib><creatorcontrib>Nadeau, Colby A</creatorcontrib><creatorcontrib>Aziz, Jasmine R</creatorcontrib><creatorcontrib>Nichol, Helen</creatorcontrib><creatorcontrib>Paterson, Phyllis G</creatorcontrib><creatorcontrib>Colbourne, Frederick</creatorcontrib><title>Rehabilitation Augments Hematoma Clearance and Attenuates Oxidative Injury and Ion Dyshomeostasis After Brain Hemorrhage</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>BACKGROUND AND PURPOSE—We assessed the elemental and biochemical effects of rehabilitation after intracerebral hemorrhage, with emphasis on iron-mediated oxidative stress, using a novel multimodal biospectroscopic imaging approach. METHODS—Collagenase-induced striatal hemorrhage was produced in rats that were randomized to enriched rehabilitation or control intervention starting on day 7. Animals were euthanized on day 14 or 21, a period of ongoing cell death. We used biospectroscopic imaging techniques to precisely determine elemental and molecular changes on day 14. Hemoglobin content was assessed with resonance Raman spectroscopy. X-ray fluorescence imaging mapped iron, chlorine, potassium, calcium, and zinc. Protein aggregation, a marker of oxidative stress, and the distribution of other macromolecules were assessed with Fourier transform infrared imaging. A second study estimated hematoma volume with a spectrophotometric assay at 21 days. RESULTS—In the first experiment, rehabilitation reduced hematoma hemoglobin content (P=0.004) and the amount of peri-hematoma iron (P&lt;0.001). Oxidative damage was highly localized at the hematoma/peri-hematoma border and was decreased by rehabilitation (P=0.004). Lipid content in the peri-hematoma zone was increased by rehabilitation (P=0.016). Rehabilitation reduced the size of calcium deposits (P=0.040) and attenuated persistent dyshomeostasis of Cl (P&lt;0.001) but not K (P=0.060). The second study confirmed that rehabilitation decreased hematoma volume (P=0.024). CONCLUSIONS—Rehabilitation accelerated clearance of toxic blood components and decreased chronic oxidative stress. As well, rehabilitation attenuated persistent ion dyshomeostasis. These novel effects may underlie rehabilitation-induced neuroprotection and improved recovery of function. 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Lipid content in the peri-hematoma zone was increased by rehabilitation (P=0.016). Rehabilitation reduced the size of calcium deposits (P=0.040) and attenuated persistent dyshomeostasis of Cl (P&lt;0.001) but not K (P=0.060). The second study confirmed that rehabilitation decreased hematoma volume (P=0.024). CONCLUSIONS—Rehabilitation accelerated clearance of toxic blood components and decreased chronic oxidative stress. As well, rehabilitation attenuated persistent ion dyshomeostasis. These novel effects may underlie rehabilitation-induced neuroprotection and improved recovery of function. Pharmacotherapies targeting these mechanisms may further improve outcome.</abstract><cop>United States</cop><pub>American Heart Association, Inc</pub><pmid>27899761</pmid><doi>10.1161/STROKEAHA.116.015404</doi><tpages>9</tpages><oa>free_for_read</oa></addata></record>
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source Alma/SFX Local Collection
subjects Animals
Cerebral Hemorrhage - metabolism
Cerebral Hemorrhage - rehabilitation
Hematoma - metabolism
Hematoma - rehabilitation
Iron - analysis
Iron - metabolism
Male
Oxidative Stress - physiology
Rats
Rats, Sprague-Dawley
Spectrometry, X-Ray Emission - methods
Spectrum Analysis, Raman - methods
title Rehabilitation Augments Hematoma Clearance and Attenuates Oxidative Injury and Ion Dyshomeostasis After Brain Hemorrhage
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