Brain electrical activity during combined hypoxemia and hypoperfusion in anesthetized rats
In order to investigate the effects of moderate hypoxemia on brain electrical activity and the consequences of an altered cerebro-vascular response to hypoxemia, we recorded changes in electrical activity of the brain in anesthetized rats following unilateral carotid artery ligation (UCAL). In these...
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| Veröffentlicht in: | Respiration physiology 2002, Vol.129 (3), p.375-384 |
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| creator | Wuyam, B Bourlier, V Pépin, J.L Payen, J.F Lévy, P |
| description | In order to investigate the effects of moderate hypoxemia on brain electrical activity and the consequences of an altered cerebro-vascular response to hypoxemia, we recorded changes in electrical activity of the brain in anesthetized rats following unilateral carotid artery ligation (UCAL). In these animals, on the clamped side, cerebral blood flow, whilst normal during normoxia, shows less augmentation during hypoxemia. Six anesthetized (Halothane) Sprague–Dawley rats with UCAL were studied during 20 min periods of baseline (F
i
O
2
=30%), hypoxemia (F
i
O
2
=9.5%) and recovery (F
i
O
2
=30%): mean arterial pressure of oxygen (P
a
O
2
) achieved was 177.0, 37.6 and 160.1 mmHg, respectively. A significant decrease in the frequencies of the ECoG was observed bilaterally during hypoxemia: centroid frequency (fc)=3.37±0.14 and 2.85±0.13 Hz on the intact and clamped hemisphere respectively during hypoxemia versus fc=4.09±0.20 Hz (mean±S.E.M.) during baseline, which was not reversed during recovery (3.27±0.11 Hz) (ANOVA,
P |
| doi_str_mv | 10.1016/S0034-5687(01)00319-X |
| format | Article |
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i
O
2
=30%), hypoxemia (F
i
O
2
=9.5%) and recovery (F
i
O
2
=30%): mean arterial pressure of oxygen (P
a
O
2
) achieved was 177.0, 37.6 and 160.1 mmHg, respectively. A significant decrease in the frequencies of the ECoG was observed bilaterally during hypoxemia: centroid frequency (fc)=3.37±0.14 and 2.85±0.13 Hz on the intact and clamped hemisphere respectively during hypoxemia versus fc=4.09±0.20 Hz (mean±S.E.M.) during baseline, which was not reversed during recovery (3.27±0.11 Hz) (ANOVA,
P<0.01). The total power of the signal (Pw) was unaffected on the intact hemisphere but diminished on the clamped side during hypoxemia. Our results show that a significant slowing of ECoG is observed during hypoxemia of moderate intensity (40 mmHg) even when cerebro-vascular response to hypoxemia is preserved and that total power of the ECoG signal is severely diminished when the cerebro-vascular response to hypoxemia is impaired.</description><identifier>ISSN: 0034-5687</identifier><identifier>DOI: 10.1016/S0034-5687(01)00319-X</identifier><identifier>PMID: 11788140</identifier><identifier>CODEN: RSPYAK</identifier><language>eng</language><publisher>Shannon: Elsevier B.V</publisher><subject>Animals ; Biological and medical sciences ; Brain - physiopathology ; Brain Ischemia - complications ; Brain Ischemia - physiopathology ; Carotid Arteries ; Carotid artery, ligation ; Electrical activity, brain ; Electrophysiology ; Female ; Homeostasis ; Hypoxia - complications ; Hypoxia - physiopathology ; Hypoxia, brain ; Ligation ; Mammals, rat ; Medical sciences ; Perfusion, brain hypoperfusion ; Pneumology ; Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases ; Rats ; Rats, Inbred Strains ; Reference Values ; Time Factors</subject><ispartof>Respiration physiology, 2002, Vol.129 (3), p.375-384</ispartof><rights>2002 Elsevier Science B.V.</rights><rights>2002 INIST-CNRS</rights><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c391t-59a86cd5870aaa14c51afa99b339085eaf54d73a6fed70977349c6bf2067ea1b3</citedby><cites>FETCH-LOGICAL-c391t-59a86cd5870aaa14c51afa99b339085eaf54d73a6fed70977349c6bf2067ea1b3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,4024,27923,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=13424010$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/11788140$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Wuyam, B</creatorcontrib><creatorcontrib>Bourlier, V</creatorcontrib><creatorcontrib>Pépin, J.L</creatorcontrib><creatorcontrib>Payen, J.F</creatorcontrib><creatorcontrib>Lévy, P</creatorcontrib><title>Brain electrical activity during combined hypoxemia and hypoperfusion in anesthetized rats</title><title>Respiration physiology</title><addtitle>Respir Physiol</addtitle><description>In order to investigate the effects of moderate hypoxemia on brain electrical activity and the consequences of an altered cerebro-vascular response to hypoxemia, we recorded changes in electrical activity of the brain in anesthetized rats following unilateral carotid artery ligation (UCAL). In these animals, on the clamped side, cerebral blood flow, whilst normal during normoxia, shows less augmentation during hypoxemia. Six anesthetized (Halothane) Sprague–Dawley rats with UCAL were studied during 20 min periods of baseline (F
i
O
2
=30%), hypoxemia (F
i
O
2
=9.5%) and recovery (F
i
O
2
=30%): mean arterial pressure of oxygen (P
a
O
2
) achieved was 177.0, 37.6 and 160.1 mmHg, respectively. A significant decrease in the frequencies of the ECoG was observed bilaterally during hypoxemia: centroid frequency (fc)=3.37±0.14 and 2.85±0.13 Hz on the intact and clamped hemisphere respectively during hypoxemia versus fc=4.09±0.20 Hz (mean±S.E.M.) during baseline, which was not reversed during recovery (3.27±0.11 Hz) (ANOVA,
P<0.01). The total power of the signal (Pw) was unaffected on the intact hemisphere but diminished on the clamped side during hypoxemia. Our results show that a significant slowing of ECoG is observed during hypoxemia of moderate intensity (40 mmHg) even when cerebro-vascular response to hypoxemia is preserved and that total power of the ECoG signal is severely diminished when the cerebro-vascular response to hypoxemia is impaired.</description><subject>Animals</subject><subject>Biological and medical sciences</subject><subject>Brain - physiopathology</subject><subject>Brain Ischemia - complications</subject><subject>Brain Ischemia - physiopathology</subject><subject>Carotid Arteries</subject><subject>Carotid artery, ligation</subject><subject>Electrical activity, brain</subject><subject>Electrophysiology</subject><subject>Female</subject><subject>Homeostasis</subject><subject>Hypoxia - complications</subject><subject>Hypoxia - physiopathology</subject><subject>Hypoxia, brain</subject><subject>Ligation</subject><subject>Mammals, rat</subject><subject>Medical sciences</subject><subject>Perfusion, brain hypoperfusion</subject><subject>Pneumology</subject><subject>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</subject><subject>Rats</subject><subject>Rats, Inbred Strains</subject><subject>Reference Values</subject><subject>Time Factors</subject><issn>0034-5687</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2002</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqFkMtOwzAQRb0A0VL4BFA2IFgE7DzsZIWg4iUhsQCkio01cSbUKI9iJxXl63GbiC5ZWdc6M74-hBwxesEo45cvlIaRH_NEnFF27gJL_dkOGf9dj8i-tZ_UZU75HhkxJpKERXRM3m8M6NrDElVrtILSA9XqpW5XXt4ZXX94qqkyXWPuzVeL5hsrDR7UfVqgKTqrm9pzK6BG286x1T-ONdDaA7JbQGnxcDgn5O3u9nX64D893z9Or598Faas9eMUEq7yOBEUAFikYgYFpGkWhilNYoQijnIRAi8wFzQVIoxSxbMioFwgsCyckNN-78I0X50rISttFZala9R0Vgr3UR6wwIFxDyrTWGuwkAujKzAryahci5QbkXJtTFImNyLlzM0dDw90WYX5dmqw6ICTAQDrFBYGaqXtlgujIKJszV31HDodS41GWqWxVphr4_zLvNH_VPkFRzSTcg</recordid><startdate>2002</startdate><enddate>2002</enddate><creator>Wuyam, B</creator><creator>Bourlier, V</creator><creator>Pépin, J.L</creator><creator>Payen, J.F</creator><creator>Lévy, P</creator><general>Elsevier B.V</general><general>Elsevier</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>2002</creationdate><title>Brain electrical activity during combined hypoxemia and hypoperfusion in anesthetized rats</title><author>Wuyam, B ; Bourlier, V ; Pépin, J.L ; Payen, J.F ; Lévy, P</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c391t-59a86cd5870aaa14c51afa99b339085eaf54d73a6fed70977349c6bf2067ea1b3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2002</creationdate><topic>Animals</topic><topic>Biological and medical sciences</topic><topic>Brain - physiopathology</topic><topic>Brain Ischemia - complications</topic><topic>Brain Ischemia - physiopathology</topic><topic>Carotid Arteries</topic><topic>Carotid artery, ligation</topic><topic>Electrical activity, brain</topic><topic>Electrophysiology</topic><topic>Female</topic><topic>Homeostasis</topic><topic>Hypoxia - complications</topic><topic>Hypoxia - physiopathology</topic><topic>Hypoxia, brain</topic><topic>Ligation</topic><topic>Mammals, rat</topic><topic>Medical sciences</topic><topic>Perfusion, brain hypoperfusion</topic><topic>Pneumology</topic><topic>Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases</topic><topic>Rats</topic><topic>Rats, Inbred Strains</topic><topic>Reference Values</topic><topic>Time Factors</topic><toplevel>online_resources</toplevel><creatorcontrib>Wuyam, B</creatorcontrib><creatorcontrib>Bourlier, V</creatorcontrib><creatorcontrib>Pépin, J.L</creatorcontrib><creatorcontrib>Payen, J.F</creatorcontrib><creatorcontrib>Lévy, P</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>Respiration physiology</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Wuyam, B</au><au>Bourlier, V</au><au>Pépin, J.L</au><au>Payen, J.F</au><au>Lévy, P</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Brain electrical activity during combined hypoxemia and hypoperfusion in anesthetized rats</atitle><jtitle>Respiration physiology</jtitle><addtitle>Respir Physiol</addtitle><date>2002</date><risdate>2002</risdate><volume>129</volume><issue>3</issue><spage>375</spage><epage>384</epage><pages>375-384</pages><issn>0034-5687</issn><coden>RSPYAK</coden><abstract>In order to investigate the effects of moderate hypoxemia on brain electrical activity and the consequences of an altered cerebro-vascular response to hypoxemia, we recorded changes in electrical activity of the brain in anesthetized rats following unilateral carotid artery ligation (UCAL). In these animals, on the clamped side, cerebral blood flow, whilst normal during normoxia, shows less augmentation during hypoxemia. Six anesthetized (Halothane) Sprague–Dawley rats with UCAL were studied during 20 min periods of baseline (F
i
O
2
=30%), hypoxemia (F
i
O
2
=9.5%) and recovery (F
i
O
2
=30%): mean arterial pressure of oxygen (P
a
O
2
) achieved was 177.0, 37.6 and 160.1 mmHg, respectively. A significant decrease in the frequencies of the ECoG was observed bilaterally during hypoxemia: centroid frequency (fc)=3.37±0.14 and 2.85±0.13 Hz on the intact and clamped hemisphere respectively during hypoxemia versus fc=4.09±0.20 Hz (mean±S.E.M.) during baseline, which was not reversed during recovery (3.27±0.11 Hz) (ANOVA,
P<0.01). The total power of the signal (Pw) was unaffected on the intact hemisphere but diminished on the clamped side during hypoxemia. Our results show that a significant slowing of ECoG is observed during hypoxemia of moderate intensity (40 mmHg) even when cerebro-vascular response to hypoxemia is preserved and that total power of the ECoG signal is severely diminished when the cerebro-vascular response to hypoxemia is impaired.</abstract><cop>Shannon</cop><cop>Amsterdam</cop><pub>Elsevier B.V</pub><pmid>11788140</pmid><doi>10.1016/S0034-5687(01)00319-X</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals Biological and medical sciences Brain - physiopathology Brain Ischemia - complications Brain Ischemia - physiopathology Carotid Arteries Carotid artery, ligation Electrical activity, brain Electrophysiology Female Homeostasis Hypoxia - complications Hypoxia - physiopathology Hypoxia, brain Ligation Mammals, rat Medical sciences Perfusion, brain hypoperfusion Pneumology Pulmonary hypertension. Acute cor pulmonale. Pulmonary embolism. Pulmonary vascular diseases Rats Rats, Inbred Strains Reference Values Time Factors |
| title | Brain electrical activity during combined hypoxemia and hypoperfusion in anesthetized rats |
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