A rapid redistribution of hydrogen ions is associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion
T. P. Obrenovitch, D. Scheller, T. Matsumoto, F. Tegtmeier, M. Holler and L. Symon Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, United Kingdom. 1. The aim of this study was to examine the rapid changes in extracellular hydrogen ion activity [( H+]o or pHo) which a...
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creator | Obrenovitch, T. P Scheller, D Matsumoto, T Tegtmeier, F Holler, M Symon, L |
description | T. P. Obrenovitch, D. Scheller, T. Matsumoto, F. Tegtmeier, M. Holler and L. Symon
Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, United Kingdom.
1. The aim of this study was to examine the rapid changes in extracellular
hydrogen ion activity [( H+]o or pHo) which are associated with
depolarization and repolarization subsequent to cerebral ischemia
reperfusion. Two parallel studies were performed with different rat models
of ischemia: repetitive severe ischemia produced in anesthetized animals by
occlusion of the vertebral and carotid arteries and temporary interruption
of blood flow in isolated brain. [H+]o and direct current potential (DC
potential) were recorded simultaneously in all experiments. Examination of
these two parameters was supplemented by recording tissue concentration of
carbon dioxide (PtCO2) in the four-vessel occlusion model and assaying
major metabolites involved in energy production in experiments with
isolated brains. 2. Measurements of [H+]o during ischemia consistently
revealed a steady increase of [H+]o on which was superimposed an abrupt and
transient fall in [H+]o closely related to the occurrence of the fast
negative shift of DC potential characterizing brain-cell depolarization.
Analysis of the relationship between the magnitude of the transient fall in
H+ and the level of [H+]o at which this occurred showed that the amplitude
of the transient fall in H+ increased with tissue acidosis. 3. We propose
that this phenomenon is indirect evidence that rapid transfer of acid
equivalents occurs across the plasmalemma, concomitantly to its
depolarization. Both events probably result from a common cause, i.e.,
nonspecific increase of the cell-membrane permeability to ions subsequent
to opening of membrane channels. 4. Early on during recirculation, an
acidotic [H+]o shift associated with membrane repolarization was clearly
visible whenever the ionic gradients recovered rapidly. |
doi_str_mv | 10.1152/jn.1990.64.4.1125 |
format | Article |
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Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, United Kingdom.
1. The aim of this study was to examine the rapid changes in extracellular
hydrogen ion activity [( H+]o or pHo) which are associated with
depolarization and repolarization subsequent to cerebral ischemia
reperfusion. Two parallel studies were performed with different rat models
of ischemia: repetitive severe ischemia produced in anesthetized animals by
occlusion of the vertebral and carotid arteries and temporary interruption
of blood flow in isolated brain. [H+]o and direct current potential (DC
potential) were recorded simultaneously in all experiments. Examination of
these two parameters was supplemented by recording tissue concentration of
carbon dioxide (PtCO2) in the four-vessel occlusion model and assaying
major metabolites involved in energy production in experiments with
isolated brains. 2. Measurements of [H+]o during ischemia consistently
revealed a steady increase of [H+]o on which was superimposed an abrupt and
transient fall in [H+]o closely related to the occurrence of the fast
negative shift of DC potential characterizing brain-cell depolarization.
Analysis of the relationship between the magnitude of the transient fall in
H+ and the level of [H+]o at which this occurred showed that the amplitude
of the transient fall in H+ increased with tissue acidosis. 3. We propose
that this phenomenon is indirect evidence that rapid transfer of acid
equivalents occurs across the plasmalemma, concomitantly to its
depolarization. Both events probably result from a common cause, i.e.,
nonspecific increase of the cell-membrane permeability to ions subsequent
to opening of membrane channels. 4. Early on during recirculation, an
acidotic [H+]o shift associated with membrane repolarization was clearly
visible whenever the ionic gradients recovered rapidly.</description><identifier>ISSN: 0022-3077</identifier><identifier>EISSN: 1522-1598</identifier><identifier>DOI: 10.1152/jn.1990.64.4.1125</identifier><identifier>PMID: 2124259</identifier><identifier>CODEN: JONEA4</identifier><language>eng</language><publisher>Bethesda, MD: Am Phys Soc</publisher><subject>Acidosis - metabolism ; Animals ; Biochemistry and metabolism ; Biological and medical sciences ; Brain Chemistry ; Brain Ischemia - metabolism ; Carbon Dioxide - metabolism ; Central nervous system ; Electrophysiology ; Fundamental and applied biological sciences. Psychology ; Glucose - metabolism ; Hydrogen - metabolism ; Hypoxia, Brain - physiopathology ; In Vitro Techniques ; Lactates - metabolism ; Male ; Rats ; Rats, Inbred Strains ; Reperfusion ; Vertebrates: nervous system and sense organs</subject><ispartof>Journal of neurophysiology, 1990-10, Vol.64 (4), p.1125-1133</ispartof><rights>1991 INIST-CNRS</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c389t-edc3b8ff9c4e32addd6abeca798dc3f96283f433e2dbef10400f55266db551313</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>315,781,785,27929,27930</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=19393074$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/2124259$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Obrenovitch, T. P</creatorcontrib><creatorcontrib>Scheller, D</creatorcontrib><creatorcontrib>Matsumoto, T</creatorcontrib><creatorcontrib>Tegtmeier, F</creatorcontrib><creatorcontrib>Holler, M</creatorcontrib><creatorcontrib>Symon, L</creatorcontrib><title>A rapid redistribution of hydrogen ions is associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion</title><title>Journal of neurophysiology</title><addtitle>J Neurophysiol</addtitle><description>T. P. Obrenovitch, D. Scheller, T. Matsumoto, F. Tegtmeier, M. Holler and L. Symon
Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, United Kingdom.
1. The aim of this study was to examine the rapid changes in extracellular
hydrogen ion activity [( H+]o or pHo) which are associated with
depolarization and repolarization subsequent to cerebral ischemia
reperfusion. Two parallel studies were performed with different rat models
of ischemia: repetitive severe ischemia produced in anesthetized animals by
occlusion of the vertebral and carotid arteries and temporary interruption
of blood flow in isolated brain. [H+]o and direct current potential (DC
potential) were recorded simultaneously in all experiments. Examination of
these two parameters was supplemented by recording tissue concentration of
carbon dioxide (PtCO2) in the four-vessel occlusion model and assaying
major metabolites involved in energy production in experiments with
isolated brains. 2. Measurements of [H+]o during ischemia consistently
revealed a steady increase of [H+]o on which was superimposed an abrupt and
transient fall in [H+]o closely related to the occurrence of the fast
negative shift of DC potential characterizing brain-cell depolarization.
Analysis of the relationship between the magnitude of the transient fall in
H+ and the level of [H+]o at which this occurred showed that the amplitude
of the transient fall in H+ increased with tissue acidosis. 3. We propose
that this phenomenon is indirect evidence that rapid transfer of acid
equivalents occurs across the plasmalemma, concomitantly to its
depolarization. Both events probably result from a common cause, i.e.,
nonspecific increase of the cell-membrane permeability to ions subsequent
to opening of membrane channels. 4. Early on during recirculation, an
acidotic [H+]o shift associated with membrane repolarization was clearly
visible whenever the ionic gradients recovered rapidly.</description><subject>Acidosis - metabolism</subject><subject>Animals</subject><subject>Biochemistry and metabolism</subject><subject>Biological and medical sciences</subject><subject>Brain Chemistry</subject><subject>Brain Ischemia - metabolism</subject><subject>Carbon Dioxide - metabolism</subject><subject>Central nervous system</subject><subject>Electrophysiology</subject><subject>Fundamental and applied biological sciences. Psychology</subject><subject>Glucose - metabolism</subject><subject>Hydrogen - metabolism</subject><subject>Hypoxia, Brain - physiopathology</subject><subject>In Vitro Techniques</subject><subject>Lactates - metabolism</subject><subject>Male</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Reperfusion</subject><subject>Vertebrates: nervous system and sense organs</subject><issn>0022-3077</issn><issn>1522-1598</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>1990</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkc1u3CAUhVGVKpkmeYAuKrFJupopv7ZZRlH6I0Xqpl0jDJcxI49xwFY0eYI-dnFn1KirroBzv3vuFQeh95RsKJXs027YUKXIphIbURQm36BV0dmaStWcoRUh5c5JXV-gdznvCCG1JOwcnTPKBJNqhX7d4WTG4HACF_KUQjtPIQ44etwdXIpbGHB5ZxwyNjlHG8wEDj-HqcMOxtibFF7MnxYzLC7_SHluMzzNMEx4ithCgjaZvnjZDvbBLDgkP-fCXqG33vQZrk_nJfr5-eHH_df14_cv3-7vHteWN2pag7O8bbxXVgBnxjlXmRasqVVTKl5VrOFecA7MteApEYR4KVlVuVZKyim_RLdH3zHFslme9L6sA31vBohz1g2hleJc_hekslaM1nUB6RG0KeacwOsxhb1JB02JXmLSu0EvMelKaKGXmErPh5P53O7B_e045VLqN6e6ydb0PpnBhvxqrLgqsYrCfTxyXdh2zyGBHrtD-c4-bg_L2NeJvwE3kq1H</recordid><startdate>19901001</startdate><enddate>19901001</enddate><creator>Obrenovitch, T. P</creator><creator>Scheller, D</creator><creator>Matsumoto, T</creator><creator>Tegtmeier, F</creator><creator>Holler, M</creator><creator>Symon, L</creator><general>Am Phys Soc</general><general>American Physiological Society</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>19901001</creationdate><title>A rapid redistribution of hydrogen ions is associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion</title><author>Obrenovitch, T. P ; Scheller, D ; Matsumoto, T ; Tegtmeier, F ; Holler, M ; Symon, L</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c389t-edc3b8ff9c4e32addd6abeca798dc3f96283f433e2dbef10400f55266db551313</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1990</creationdate><topic>Acidosis - metabolism</topic><topic>Animals</topic><topic>Biochemistry and metabolism</topic><topic>Biological and medical sciences</topic><topic>Brain Chemistry</topic><topic>Brain Ischemia - metabolism</topic><topic>Carbon Dioxide - metabolism</topic><topic>Central nervous system</topic><topic>Electrophysiology</topic><topic>Fundamental and applied biological sciences. Psychology</topic><topic>Glucose - metabolism</topic><topic>Hydrogen - metabolism</topic><topic>Hypoxia, Brain - physiopathology</topic><topic>In Vitro Techniques</topic><topic>Lactates - metabolism</topic><topic>Male</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Reperfusion</topic><topic>Vertebrates: nervous system and sense organs</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Obrenovitch, T. P</creatorcontrib><creatorcontrib>Scheller, D</creatorcontrib><creatorcontrib>Matsumoto, T</creatorcontrib><creatorcontrib>Tegtmeier, F</creatorcontrib><creatorcontrib>Holler, M</creatorcontrib><creatorcontrib>Symon, L</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>Journal of neurophysiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Obrenovitch, T. P</au><au>Scheller, D</au><au>Matsumoto, T</au><au>Tegtmeier, F</au><au>Holler, M</au><au>Symon, L</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>A rapid redistribution of hydrogen ions is associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion</atitle><jtitle>Journal of neurophysiology</jtitle><addtitle>J Neurophysiol</addtitle><date>1990-10-01</date><risdate>1990</risdate><volume>64</volume><issue>4</issue><spage>1125</spage><epage>1133</epage><pages>1125-1133</pages><issn>0022-3077</issn><eissn>1522-1598</eissn><coden>JONEA4</coden><abstract>T. P. Obrenovitch, D. Scheller, T. Matsumoto, F. Tegtmeier, M. Holler and L. Symon
Gough-Cooper Department of Neurological Surgery, Institute of Neurology, London, United Kingdom.
1. The aim of this study was to examine the rapid changes in extracellular
hydrogen ion activity [( H+]o or pHo) which are associated with
depolarization and repolarization subsequent to cerebral ischemia
reperfusion. Two parallel studies were performed with different rat models
of ischemia: repetitive severe ischemia produced in anesthetized animals by
occlusion of the vertebral and carotid arteries and temporary interruption
of blood flow in isolated brain. [H+]o and direct current potential (DC
potential) were recorded simultaneously in all experiments. Examination of
these two parameters was supplemented by recording tissue concentration of
carbon dioxide (PtCO2) in the four-vessel occlusion model and assaying
major metabolites involved in energy production in experiments with
isolated brains. 2. Measurements of [H+]o during ischemia consistently
revealed a steady increase of [H+]o on which was superimposed an abrupt and
transient fall in [H+]o closely related to the occurrence of the fast
negative shift of DC potential characterizing brain-cell depolarization.
Analysis of the relationship between the magnitude of the transient fall in
H+ and the level of [H+]o at which this occurred showed that the amplitude
of the transient fall in H+ increased with tissue acidosis. 3. We propose
that this phenomenon is indirect evidence that rapid transfer of acid
equivalents occurs across the plasmalemma, concomitantly to its
depolarization. Both events probably result from a common cause, i.e.,
nonspecific increase of the cell-membrane permeability to ions subsequent
to opening of membrane channels. 4. Early on during recirculation, an
acidotic [H+]o shift associated with membrane repolarization was clearly
visible whenever the ionic gradients recovered rapidly.</abstract><cop>Bethesda, MD</cop><pub>Am Phys Soc</pub><pmid>2124259</pmid><doi>10.1152/jn.1990.64.4.1125</doi><tpages>9</tpages></addata></record> |
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source | MEDLINE; Alma/SFX Local Collection |
subjects | Acidosis - metabolism Animals Biochemistry and metabolism Biological and medical sciences Brain Chemistry Brain Ischemia - metabolism Carbon Dioxide - metabolism Central nervous system Electrophysiology Fundamental and applied biological sciences. Psychology Glucose - metabolism Hydrogen - metabolism Hypoxia, Brain - physiopathology In Vitro Techniques Lactates - metabolism Male Rats Rats, Inbred Strains Reperfusion Vertebrates: nervous system and sense organs |
title | A rapid redistribution of hydrogen ions is associated with depolarization and repolarization subsequent to cerebral ischemia reperfusion |
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