Correlation between brain surface potassium and glucose utilization after bilateral cerebral ischemia in the gerbil
The correlation between cerebral glucose utilization and brain surface potassium concentration (BS-K+) was studied during reperfusion following bilateral cerebral ischemia in the gerbil. Cerebral glucose utilization rate was measured by the 14C-2-deoxyglucose method and BS-K+ was continuously monito...
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Veröffentlicht in: | Stroke (1970) 1984-09, Vol.15 (5), p.851-857 |
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description | The correlation between cerebral glucose utilization and brain surface potassium concentration (BS-K+) was studied during reperfusion following bilateral cerebral ischemia in the gerbil. Cerebral glucose utilization rate was measured by the 14C-2-deoxyglucose method and BS-K+ was continuously monitored by a potassium sensitive membrane electrode. BS-K+ increased from 3.0 +/- 0.6 mM (mean +/- S.D.) before ischemia to 58.7 +/- 17.3 mM 30 minutes after the occlusion of both common carotid arteries. The rate of decline of BS-K+ after release of occlusion differed between animals. Glucose utilization rate in the cerebral cortex immediately under the potassium electrode was low but homogeneous in 7 animals while in 5 animals the metabolic pattern was heterogeneous with areas of both low and high glucose metabolism. The former animals exhibited a fast recovery of potassium flux while the latter animals showed a slow recovery. Glucose utilization rate and potassium half recovery time were linearly correlated. These studies suggest that the reason that potassium flux may not recover rapidly in postischemic brain tissue is due to the lack of sufficient energy for a rapid re-establishment of the ion gradient across the cell due to the inefficient energy production of anaerobic glycolysis. |
doi_str_mv | 10.1161/01.STR.15.5.851 |
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Cerebral glucose utilization rate was measured by the 14C-2-deoxyglucose method and BS-K+ was continuously monitored by a potassium sensitive membrane electrode. BS-K+ increased from 3.0 +/- 0.6 mM (mean +/- S.D.) before ischemia to 58.7 +/- 17.3 mM 30 minutes after the occlusion of both common carotid arteries. The rate of decline of BS-K+ after release of occlusion differed between animals. Glucose utilization rate in the cerebral cortex immediately under the potassium electrode was low but homogeneous in 7 animals while in 5 animals the metabolic pattern was heterogeneous with areas of both low and high glucose metabolism. The former animals exhibited a fast recovery of potassium flux while the latter animals showed a slow recovery. Glucose utilization rate and potassium half recovery time were linearly correlated. These studies suggest that the reason that potassium flux may not recover rapidly in postischemic brain tissue is due to the lack of sufficient energy for a rapid re-establishment of the ion gradient across the cell due to the inefficient energy production of anaerobic glycolysis.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.15.5.851</identifier><identifier>PMID: 6474537</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Animals ; Biological and medical sciences ; Brain - blood supply ; Brain - metabolism ; Brain Ischemia - metabolism ; Brain Ischemia - physiopathology ; Electroencephalography ; Gerbillinae ; Glucose - metabolism ; Male ; Medical sciences ; Neurology ; Potassium - metabolism ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 1984-09, Vol.15 (5), p.851-857</ispartof><rights>1985 INIST-CNRS</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c428t-bf5b44c0bc2357793968bd571ad62a6e5ec75d9bf8355875601b1011b821b2793</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,3688,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=9018292$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/6474537$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>CHOKI, J</creatorcontrib><creatorcontrib>GREENBERG, J</creatorcontrib><creatorcontrib>SCLARSKY, D</creatorcontrib><creatorcontrib>REIVICH, M</creatorcontrib><title>Correlation between brain surface potassium and glucose utilization after bilateral cerebral ischemia in the gerbil</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>The correlation between cerebral glucose utilization and brain surface potassium concentration (BS-K+) was studied during reperfusion following bilateral cerebral ischemia in the gerbil. Cerebral glucose utilization rate was measured by the 14C-2-deoxyglucose method and BS-K+ was continuously monitored by a potassium sensitive membrane electrode. BS-K+ increased from 3.0 +/- 0.6 mM (mean +/- S.D.) before ischemia to 58.7 +/- 17.3 mM 30 minutes after the occlusion of both common carotid arteries. The rate of decline of BS-K+ after release of occlusion differed between animals. Glucose utilization rate in the cerebral cortex immediately under the potassium electrode was low but homogeneous in 7 animals while in 5 animals the metabolic pattern was heterogeneous with areas of both low and high glucose metabolism. The former animals exhibited a fast recovery of potassium flux while the latter animals showed a slow recovery. Glucose utilization rate and potassium half recovery time were linearly correlated. These studies suggest that the reason that potassium flux may not recover rapidly in postischemic brain tissue is due to the lack of sufficient energy for a rapid re-establishment of the ion gradient across the cell due to the inefficient energy production of anaerobic glycolysis.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - blood supply</subject><subject>Brain - metabolism</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - physiopathology</subject><subject>Electroencephalography</subject><subject>Gerbillinae</subject><subject>Glucose - metabolism</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Neurology</subject><subject>Potassium - metabolism</subject><subject>Vascular diseases and vascular malformations of the nervous system</subject><issn>0039-2499</issn><issn>1524-4628</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1984</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1r3TAQxEVpSV-Tnnsq6FB6s6OVtbJ8LI9-BAKFNDkLSV4nKv54lWxK-tdX4T1yzWkW5jfDwjD2AUQNoOFSQP3r9qYGrLE2CK_YDlCqSmlpXrOdEE1XSdV1b9m7nH8LIWRj8IydadUqbNody_slJRrdGpeZe1r_EhVNLs48b2lwgfhhWV3OcZu4m3t-P25hycS3NY7x3zHnhpUS97HUUHIjD5TIPx0xhweaouOlbn0gfk-pUBfszeDGTO9Pes7uvn293f-orn9-v9p_ua6Ckmat_IBeqSB8kA22bdd02vgeW3C9lk4TUmix7_xgGkTTohbgQQB4I8HLwp-zz8feQ1r-bJRXO5WHaBzdTMuWrQHZKNT6RRCUkkobUcDLIxjSknOiwR5SnFx6tCDs0x5WgC17WECLtuxREh9P1ZufqH_mTwMU_9PJdzm4cUhuDjE_Y50AIzvZ_AcbzZP_</recordid><startdate>198409</startdate><enddate>198409</enddate><creator>CHOKI, J</creator><creator>GREENBERG, J</creator><creator>SCLARSKY, D</creator><creator>REIVICH, M</creator><general>Lippincott Williams & Wilkins</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>7TK</scope><scope>7X8</scope></search><sort><creationdate>198409</creationdate><title>Correlation between brain surface potassium and glucose utilization after bilateral cerebral ischemia in the gerbil</title><author>CHOKI, J ; GREENBERG, J ; SCLARSKY, D ; REIVICH, M</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c428t-bf5b44c0bc2357793968bd571ad62a6e5ec75d9bf8355875601b1011b821b2793</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1984</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain - blood supply</topic><topic>Brain - metabolism</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - physiopathology</topic><topic>Electroencephalography</topic><topic>Gerbillinae</topic><topic>Glucose - metabolism</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Neurology</topic><topic>Potassium - metabolism</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>CHOKI, J</creatorcontrib><creatorcontrib>GREENBERG, J</creatorcontrib><creatorcontrib>SCLARSKY, D</creatorcontrib><creatorcontrib>REIVICH, 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>Neurosciences Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>CHOKI, J</au><au>GREENBERG, J</au><au>SCLARSKY, D</au><au>REIVICH, M</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Correlation between brain surface potassium and glucose utilization after bilateral cerebral ischemia in the gerbil</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>1984-09</date><risdate>1984</risdate><volume>15</volume><issue>5</issue><spage>851</spage><epage>857</epage><pages>851-857</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>The correlation between cerebral glucose utilization and brain surface potassium concentration (BS-K+) was studied during reperfusion following bilateral cerebral ischemia in the gerbil. Cerebral glucose utilization rate was measured by the 14C-2-deoxyglucose method and BS-K+ was continuously monitored by a potassium sensitive membrane electrode. BS-K+ increased from 3.0 +/- 0.6 mM (mean +/- S.D.) before ischemia to 58.7 +/- 17.3 mM 30 minutes after the occlusion of both common carotid arteries. The rate of decline of BS-K+ after release of occlusion differed between animals. Glucose utilization rate in the cerebral cortex immediately under the potassium electrode was low but homogeneous in 7 animals while in 5 animals the metabolic pattern was heterogeneous with areas of both low and high glucose metabolism. The former animals exhibited a fast recovery of potassium flux while the latter animals showed a slow recovery. Glucose utilization rate and potassium half recovery time were linearly correlated. These studies suggest that the reason that potassium flux may not recover rapidly in postischemic brain tissue is due to the lack of sufficient energy for a rapid re-establishment of the ion gradient across the cell due to the inefficient energy production of anaerobic glycolysis.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>6474537</pmid><doi>10.1161/01.STR.15.5.851</doi><tpages>7</tpages><oa>free_for_read</oa></addata></record> |
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subjects | Animals Biological and medical sciences Brain - blood supply Brain - metabolism Brain Ischemia - metabolism Brain Ischemia - physiopathology Electroencephalography Gerbillinae Glucose - metabolism Male Medical sciences Neurology Potassium - metabolism Vascular diseases and vascular malformations of the nervous system |
title | Correlation between brain surface potassium and glucose utilization after bilateral cerebral ischemia in the gerbil |
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