Effect of hyperbaric oxygenation on the Na+, K+-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage
It is reported that CNS hemorrhage causes membrane dysfunction and may exacerbate this damage as a result of secondary ischemia or hypoxia. Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygen...
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| Veröffentlicht in: | Neurochemical research 1993-09, Vol.18 (9), p.1033-1039 |
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| creator | YUFU, K ITOH, T EDAMATSU, R MORI, A HIRAKAWA, M |
| description | It is reported that CNS hemorrhage causes membrane dysfunction and may exacerbate this damage as a result of secondary ischemia or hypoxia. Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygenation influences membrane alteration after hemorrhage. Thirty minutes after subarachnoid hemorrhage induction, rats were treated with hyperbaric oxygenation 2 ATA for 1 hour. Rats were decapitated 2 hours after subarachnoid hemorrhage induction. Na+, K(+)-ATPase activity measurement and spin-label studies were performed on crude synaptosomal membranes. Subarachnoid hemorrhage decreased Na+, K(+)-ATPase activity. Spin label studies showed that hydrophobic portions of near the membrane surface became more rigid and the mobility of the membrane protein labeled sulfhydryl groups decreased after subarachnoid hemorrhage. Hyperbaric oxygenation significantly ameliorated most of the subarachnoid hemorrhage induced alterations. We conclude that hyperbaric oxygenation may be a beneficial treatment for acute subarachnoid hemorrhage. |
| doi_str_mv | 10.1007/BF00966765 |
| format | Article |
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Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygenation influences membrane alteration after hemorrhage. Thirty minutes after subarachnoid hemorrhage induction, rats were treated with hyperbaric oxygenation 2 ATA for 1 hour. Rats were decapitated 2 hours after subarachnoid hemorrhage induction. Na+, K(+)-ATPase activity measurement and spin-label studies were performed on crude synaptosomal membranes. Subarachnoid hemorrhage decreased Na+, K(+)-ATPase activity. Spin label studies showed that hydrophobic portions of near the membrane surface became more rigid and the mobility of the membrane protein labeled sulfhydryl groups decreased after subarachnoid hemorrhage. Hyperbaric oxygenation significantly ameliorated most of the subarachnoid hemorrhage induced alterations. We conclude that hyperbaric oxygenation may be a beneficial treatment for acute subarachnoid hemorrhage.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Cerebral Cortex - drug effects</subject><subject>Hyperbaric Oxygenation</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Membrane Fluidity - drug effects</subject><subject>Neurology</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Sodium-Potassium-Exchanging ATPase - drug effects</subject><subject>Subarachnoid Hemorrhage - drug therapy</subject><subject>Subarachnoid Hemorrhage - enzymology</subject><subject>Synaptic Membranes - drug effects</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0364-3190</issn><issn>1573-6903</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1993</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpFkU9v1DAQxS1EVZbChTuSD4gDJTD-Eyc-lqqFqlXhUM6RY4-boCTe2o7U_R58YFx1tUgjzeH99GbmDSHvGHxhAM3Xb5cAWqlG1S_IhtWNqJQG8ZJsQChZCabhFXmd0h-AgnN2TI5bLnjDYUP-XniPNtPg6bDbYuxNHC0Nj7t7XEwew0JL5QHprTn9TK9Pq7O7XyYhNYujM859NAtSP62jG_PuycVixD4GG2IerZkOUKLGZ4wUH8uUccYlFzGtZZ6xwxJGRwecQ4yDucc35MibKeHbfT8hvy8v7s5_VDc_v1-dn91UVjCWK44GhOylEpqrBqTppfbacN7KWiloda-dF9JZaJxohOuddCCBcdYiyroVJ-Tjs-82hocVU-7mMVmcprJvWFPXKKgZq6GAn55BG0NKEX23LTeYuOsYdE8v6P6_oMDv965rP6M7oPvMi_5hr5tUEvIlHTumAyY15yC1-Ael1o56</recordid><startdate>19930901</startdate><enddate>19930901</enddate><creator>YUFU, K</creator><creator>ITOH, T</creator><creator>EDAMATSU, R</creator><creator>MORI, A</creator><creator>HIRAKAWA, M</creator><general>Springer</general><scope>IQODW</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>19930901</creationdate><title>Effect of hyperbaric oxygenation on the Na+, K+-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage</title><author>YUFU, K ; ITOH, T ; EDAMATSU, R ; MORI, A ; HIRAKAWA, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c311t-2ea034b463926704ab49f9a2284566089b9df34dc07d373dbd4d0401218ee4583</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1993</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Cerebral Cortex - drug effects</topic><topic>Hyperbaric Oxygenation</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Membrane Fluidity - drug effects</topic><topic>Neurology</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Sodium-Potassium-Exchanging ATPase - drug effects</topic><topic>Subarachnoid Hemorrhage - drug therapy</topic><topic>Subarachnoid Hemorrhage - enzymology</topic><topic>Synaptic Membranes - drug effects</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YUFU, K</creatorcontrib><creatorcontrib>ITOH, T</creatorcontrib><creatorcontrib>EDAMATSU, R</creatorcontrib><creatorcontrib>MORI, A</creatorcontrib><creatorcontrib>HIRAKAWA, M</creatorcontrib><collection>Pascal-Francis</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Neurochemical research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YUFU, K</au><au>ITOH, T</au><au>EDAMATSU, R</au><au>MORI, A</au><au>HIRAKAWA, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Effect of hyperbaric oxygenation on the Na+, K+-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage</atitle><jtitle>Neurochemical research</jtitle><addtitle>Neurochem Res</addtitle><date>1993-09-01</date><risdate>1993</risdate><volume>18</volume><issue>9</issue><spage>1033</spage><epage>1039</epage><pages>1033-1039</pages><issn>0364-3190</issn><eissn>1573-6903</eissn><coden>NEREDZ</coden><abstract>It is reported that CNS hemorrhage causes membrane dysfunction and may exacerbate this damage as a result of secondary ischemia or hypoxia. Since hyperbaric oxygenation improves oxygen metabolism, it may reduce this membrane damage. The present study was conducted to reveal whether hyperbaric oxygenation influences membrane alteration after hemorrhage. Thirty minutes after subarachnoid hemorrhage induction, rats were treated with hyperbaric oxygenation 2 ATA for 1 hour. Rats were decapitated 2 hours after subarachnoid hemorrhage induction. Na+, K(+)-ATPase activity measurement and spin-label studies were performed on crude synaptosomal membranes. Subarachnoid hemorrhage decreased Na+, K(+)-ATPase activity. Spin label studies showed that hydrophobic portions of near the membrane surface became more rigid and the mobility of the membrane protein labeled sulfhydryl groups decreased after subarachnoid hemorrhage. Hyperbaric oxygenation significantly ameliorated most of the subarachnoid hemorrhage induced alterations. We conclude that hyperbaric oxygenation may be a beneficial treatment for acute subarachnoid hemorrhage.</abstract><cop>New York, NY</cop><pub>Springer</pub><pmid>8232720</pmid><doi>10.1007/BF00966765</doi><tpages>7</tpages></addata></record> |
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| ispartof | Neurochemical research, 1993-09, Vol.18 (9), p.1033-1039 |
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| subjects | Animals Biological and medical sciences Cerebral Cortex - drug effects Hyperbaric Oxygenation Male Medical sciences Membrane Fluidity - drug effects Neurology Rats Rats, Sprague-Dawley Sodium-Potassium-Exchanging ATPase - drug effects Subarachnoid Hemorrhage - drug therapy Subarachnoid Hemorrhage - enzymology Synaptic Membranes - drug effects Vascular diseases and vascular malformations of the nervous system |
| title | Effect of hyperbaric oxygenation on the Na+, K+-ATPase and membrane fluidity of cerebrocortical membranes after experimental subarachnoid hemorrhage |
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