| Endothelial cell swelling and brain perfusion. | |
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MedLine Citation:
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PMID: 9191694 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
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BACKGROUND: Whereas the contribution of glial swelling to no-reflow conditions in the ischemic penumbra or during reperfusion after after global ischemia is widely discussed, little is known about cell volume control of endothelial cells under reperfusion conditions. METHODS: The effect of extracellular acidosis-a key mediator of secondary brain damage-on cell volume was studied in the GM7373 endothelial cell line. Experiments were performed at pH = 6.0 in the presence or absence of bicarbonate, and during exposure to inhibitors of specific transport systems such as ethyl isopropyl amiloride or 4,4'-diisothiocyanatostilbene-2,2'-disulfonic acid. RESULTS: Endothelial swelling to 111.1 +/- 3.4% was found at pHe = 6.0 in bicarbonate-buffered media. In hydroxyethyl piperin ethanesulfonic acid-buffered media, swelling was only 107.9 +/- 0.3%. 4,4'-Diisothiocyanatostilbene-2,2'-disulfonic acid reduced swelling to 102.8 +/- 0.6% in bicarbonate media, whereas swelling was completely prevented in the presence of ethyl isopropyl amiloride in hydroxyethyl piperin ethanesulfonic acid-buffered media. CONCLUSIONS: Endothelial swelling can be expected to occur in severely ischemic tissue sections and may then advance no-reflow. Therapeutic strategies should be established to prevent acidosis-induced endothelial swelling, e.g., by specific antagonists of the transport systems involved, or to reduce swelling by osmotic treatment such as hypertonic-hyperoncotic solutions. |
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Authors:
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O Kempski; S Behmanesh |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: The Journal of trauma Volume: 42 ISSN: 0022-5282 ISO Abbreviation: J Trauma Publication Date: 1997 May |
Date Detail:
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Created Date: 1997-07-10 Completed Date: 1997-07-10 Revised Date: 2004-11-17 |
Medline Journal Info:
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Nlm Unique ID: 0376373 Medline TA: J Trauma Country: UNITED STATES |
Other Details:
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Languages: eng Pagination: S38-40 Citation Subset: AIM; IM |
Affiliation:
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Institute for Neurosurgical Pathophysiology, Johannes Gutenberg-University, Mainz, Germany. |
Export Citation:
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APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
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Acidosis
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metabolism* Animals Brain Ischemia / metabolism*, pathology, physiopathology Cattle Cell Line Cell Membrane Permeability Cell Size Cerebrovascular Circulation* Endothelium, Vascular / pathology* Hydrogen-Ion Concentration Microcirculation* Reperfusion Injury / metabolism* |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
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