Cerebral hematocrit decreases with hemodynamic compromise in carotid artery occlusion : A PET study
This study investigated whether in patients with internal carotid artery occlusion the regional cerebral hematocrit correlates with cerebral hemodynamics or metabolic state and, if so, how the regional cerebral hematocrit changes in the hemodynamically compromised region. We used positron emission t...
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| Veröffentlicht in: | Stroke (1970) 1998, Vol.29 (1), p.98-103 |
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| creator | YAMAUCHI, H FUKUYAMA, H NAGAHAMA, Y KATSUMI, Y OKAZAWA, H |
| description | This study investigated whether in patients with internal carotid artery occlusion the regional cerebral hematocrit correlates with cerebral hemodynamics or metabolic state and, if so, how the regional cerebral hematocrit changes in the hemodynamically compromised region.
We used positron emission tomography to study seven patients with unilateral internal carotid artery occlusion and no cortical infarction in the chronic stage. The distributions of red blood cell and plasma volumes were assessed using oxygen-15-labeled carbon monoxide and copper-62-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The calculated hematocrit value was compared with the hemodynamic and metabolic parameters measured with the oxygen-15 steady-state technique.
In the cerebral cortex, the value of the cerebral hematocrit varied but was correlated with the hemodynamic and metabolic status. Stepwise regression analysis revealed that the large vessel hematocrit, the cerebral metabolic rate of oxygen, and the cerebral blood flow or the oxygen extraction fraction accounted for a significant proportion of variance of the cerebral hematocrit. The oxygen extraction fraction and the cerebral metabolic rate of oxygen negatively correlated with the cerebral hematocrit, whereas the cerebral blood flow correlated positively: patients with reduced blood supply relative to metabolic demand (decreased blood flow with increased oxygen extraction fraction) showed low hematocrit values.
In carotid artery occlusion in the chronic stage, regional cerebral hematocrit may vary according to cerebral hemodynamics and metabolic status. Regional cerebral hematocrit may decrease with hemodynamic compromise unless oxygen metabolism concomitantly decreases. |
| doi_str_mv | 10.1161/01.STR.29.1.98 |
| format | Article |
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We used positron emission tomography to study seven patients with unilateral internal carotid artery occlusion and no cortical infarction in the chronic stage. The distributions of red blood cell and plasma volumes were assessed using oxygen-15-labeled carbon monoxide and copper-62-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The calculated hematocrit value was compared with the hemodynamic and metabolic parameters measured with the oxygen-15 steady-state technique.
In the cerebral cortex, the value of the cerebral hematocrit varied but was correlated with the hemodynamic and metabolic status. Stepwise regression analysis revealed that the large vessel hematocrit, the cerebral metabolic rate of oxygen, and the cerebral blood flow or the oxygen extraction fraction accounted for a significant proportion of variance of the cerebral hematocrit. The oxygen extraction fraction and the cerebral metabolic rate of oxygen negatively correlated with the cerebral hematocrit, whereas the cerebral blood flow correlated positively: patients with reduced blood supply relative to metabolic demand (decreased blood flow with increased oxygen extraction fraction) showed low hematocrit values.
In carotid artery occlusion in the chronic stage, regional cerebral hematocrit may vary according to cerebral hemodynamics and metabolic status. Regional cerebral hematocrit may decrease with hemodynamic compromise unless oxygen metabolism concomitantly decreases.</description><identifier>ISSN: 0039-2499</identifier><identifier>EISSN: 1524-4628</identifier><identifier>DOI: 10.1161/01.STR.29.1.98</identifier><identifier>PMID: 9445336</identifier><identifier>CODEN: SJCCA7</identifier><language>eng</language><publisher>Hagerstown, MD: Lippincott Williams & Wilkins</publisher><subject>Aged ; Biological and medical sciences ; Brain - diagnostic imaging ; Brain - metabolism ; Brain - physiopathology ; Brain Ischemia - blood ; Brain Ischemia - diagnostic imaging ; Brain Ischemia - physiopathology ; Carbon Monoxide ; Carotid Artery Diseases - blood ; Carotid Artery Diseases - diagnostic imaging ; Carotid Artery Diseases - physiopathology ; Carotid Artery, Internal - diagnostic imaging ; Carotid Artery, Internal - physiopathology ; Cerebral Cortex - diagnostic imaging ; Cerebral Cortex - metabolism ; Cerebral Cortex - physiopathology ; Cerebral Infarction - blood ; Cerebral Infarction - diagnostic imaging ; Cerebral Infarction - physiopathology ; Cerebrovascular Circulation - physiology ; Chronic Disease ; Copper Radioisotopes ; Female ; Hematocrit ; Hemodynamics ; Humans ; Male ; Medical sciences ; Middle Aged ; Neurology ; Oxygen Consumption - physiology ; Oxygen Radioisotopes ; Plasma Volume ; Radiopharmaceuticals ; Regression Analysis ; Serum Albumin ; Thiosemicarbazones ; Tomography, Emission-Computed ; Vascular diseases and vascular malformations of the nervous system</subject><ispartof>Stroke (1970), 1998, Vol.29 (1), p.98-103</ispartof><rights>1998 INIST-CNRS</rights><rights>Copyright American Heart Association, Inc. Jan 1998</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><cites>FETCH-LOGICAL-c335t-d78b7ddfa1ac725ce33a0fb4a57c17d9de476ca220f92f5e05fe0039e936f5dd3</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>309,310,314,780,784,789,790,3687,4050,4051,23930,23931,25140,27924,27925</link.rule.ids><backlink>$$Uhttp://pascal-francis.inist.fr/vibad/index.php?action=getRecordDetail&idt=2135711$$DView record in Pascal Francis$$Hfree_for_read</backlink><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/9445336$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>YAMAUCHI, H</creatorcontrib><creatorcontrib>FUKUYAMA, H</creatorcontrib><creatorcontrib>NAGAHAMA, Y</creatorcontrib><creatorcontrib>KATSUMI, Y</creatorcontrib><creatorcontrib>OKAZAWA, H</creatorcontrib><title>Cerebral hematocrit decreases with hemodynamic compromise in carotid artery occlusion : A PET study</title><title>Stroke (1970)</title><addtitle>Stroke</addtitle><description>This study investigated whether in patients with internal carotid artery occlusion the regional cerebral hematocrit correlates with cerebral hemodynamics or metabolic state and, if so, how the regional cerebral hematocrit changes in the hemodynamically compromised region.
We used positron emission tomography to study seven patients with unilateral internal carotid artery occlusion and no cortical infarction in the chronic stage. The distributions of red blood cell and plasma volumes were assessed using oxygen-15-labeled carbon monoxide and copper-62-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The calculated hematocrit value was compared with the hemodynamic and metabolic parameters measured with the oxygen-15 steady-state technique.
In the cerebral cortex, the value of the cerebral hematocrit varied but was correlated with the hemodynamic and metabolic status. Stepwise regression analysis revealed that the large vessel hematocrit, the cerebral metabolic rate of oxygen, and the cerebral blood flow or the oxygen extraction fraction accounted for a significant proportion of variance of the cerebral hematocrit. The oxygen extraction fraction and the cerebral metabolic rate of oxygen negatively correlated with the cerebral hematocrit, whereas the cerebral blood flow correlated positively: patients with reduced blood supply relative to metabolic demand (decreased blood flow with increased oxygen extraction fraction) showed low hematocrit values.
In carotid artery occlusion in the chronic stage, regional cerebral hematocrit may vary according to cerebral hemodynamics and metabolic status. Regional cerebral hematocrit may decrease with hemodynamic compromise unless oxygen metabolism concomitantly decreases.</description><subject>Aged</subject><subject>Biological and medical sciences</subject><subject>Brain - diagnostic imaging</subject><subject>Brain - metabolism</subject><subject>Brain - physiopathology</subject><subject>Brain Ischemia - blood</subject><subject>Brain Ischemia - diagnostic imaging</subject><subject>Brain Ischemia - physiopathology</subject><subject>Carbon Monoxide</subject><subject>Carotid Artery Diseases - blood</subject><subject>Carotid Artery Diseases - diagnostic imaging</subject><subject>Carotid Artery Diseases - physiopathology</subject><subject>Carotid Artery, Internal - diagnostic imaging</subject><subject>Carotid Artery, Internal - physiopathology</subject><subject>Cerebral Cortex - diagnostic imaging</subject><subject>Cerebral Cortex - metabolism</subject><subject>Cerebral Cortex - physiopathology</subject><subject>Cerebral Infarction - blood</subject><subject>Cerebral Infarction - diagnostic imaging</subject><subject>Cerebral Infarction - physiopathology</subject><subject>Cerebrovascular Circulation - physiology</subject><subject>Chronic Disease</subject><subject>Copper Radioisotopes</subject><subject>Female</subject><subject>Hematocrit</subject><subject>Hemodynamics</subject><subject>Humans</subject><subject>Male</subject><subject>Medical sciences</subject><subject>Middle Aged</subject><subject>Neurology</subject><subject>Oxygen Consumption - physiology</subject><subject>Oxygen Radioisotopes</subject><subject>Plasma Volume</subject><subject>Radiopharmaceuticals</subject><subject>Regression Analysis</subject><subject>Serum Albumin</subject><subject>Thiosemicarbazones</subject><subject>Tomography, Emission-Computed</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>1998</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNpdkM1r3DAUxEVpSLdprr0VRCm92dWnZfUWlrQNBFrazVm8lZ6Igm2lkk3Y_75esuTQ0zvMb4Z5Q8h7zlrOO_6F8fbP7ncrbMtb278iG66FalQn-tdkw5i0jVDWviFva31gjAnZ63NybpXSUnYb4rdYcF9goPc4wpx9STMN6AtCxUqf0nx_VHI4TDAmT30eH0seU0WaJuqh5DkFCmXGcqDZ-2GpKU_0K72iv653tM5LOLwjZxGGipene0Huvl3vtj-a25_fb7ZXt42XUs9NMP3ehBCBgzdCe5QSWNwr0MZzE2xAZToPQrBoRdTIdMTjg2hlF3UI8oJ8fs5dG_5dsM5u7elxGGDCvFRnbGeUsnwFP_4HPuSlTGs3x60xfS90t0LtM-RLrrVgdI8ljVAOjjN3nN4x7tbpnbCOO9uvhg-n1GU_YnjBT1uv-qeTDtXDEAtMPtUXTHCpDefyH4k8jKg</recordid><startdate>1998</startdate><enddate>1998</enddate><creator>YAMAUCHI, H</creator><creator>FUKUYAMA, H</creator><creator>NAGAHAMA, Y</creator><creator>KATSUMI, Y</creator><creator>OKAZAWA, H</creator><general>Lippincott Williams & Wilkins</general><general>American Heart Association, Inc</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope></search><sort><creationdate>1998</creationdate><title>Cerebral hematocrit decreases with hemodynamic compromise in carotid artery occlusion : A PET study</title><author>YAMAUCHI, H ; FUKUYAMA, H ; NAGAHAMA, Y ; KATSUMI, Y ; OKAZAWA, H</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c335t-d78b7ddfa1ac725ce33a0fb4a57c17d9de476ca220f92f5e05fe0039e936f5dd3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>1998</creationdate><topic>Aged</topic><topic>Biological and medical sciences</topic><topic>Brain - diagnostic imaging</topic><topic>Brain - metabolism</topic><topic>Brain - physiopathology</topic><topic>Brain Ischemia - blood</topic><topic>Brain Ischemia - diagnostic imaging</topic><topic>Brain Ischemia - physiopathology</topic><topic>Carbon Monoxide</topic><topic>Carotid Artery Diseases - blood</topic><topic>Carotid Artery Diseases - diagnostic imaging</topic><topic>Carotid Artery Diseases - physiopathology</topic><topic>Carotid Artery, Internal - diagnostic imaging</topic><topic>Carotid Artery, Internal - physiopathology</topic><topic>Cerebral Cortex - diagnostic imaging</topic><topic>Cerebral Cortex - metabolism</topic><topic>Cerebral Cortex - physiopathology</topic><topic>Cerebral Infarction - blood</topic><topic>Cerebral Infarction - diagnostic imaging</topic><topic>Cerebral Infarction - physiopathology</topic><topic>Cerebrovascular Circulation - physiology</topic><topic>Chronic Disease</topic><topic>Copper Radioisotopes</topic><topic>Female</topic><topic>Hematocrit</topic><topic>Hemodynamics</topic><topic>Humans</topic><topic>Male</topic><topic>Medical sciences</topic><topic>Middle Aged</topic><topic>Neurology</topic><topic>Oxygen Consumption - physiology</topic><topic>Oxygen Radioisotopes</topic><topic>Plasma Volume</topic><topic>Radiopharmaceuticals</topic><topic>Regression Analysis</topic><topic>Serum Albumin</topic><topic>Thiosemicarbazones</topic><topic>Tomography, Emission-Computed</topic><topic>Vascular diseases and vascular malformations of the nervous system</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>YAMAUCHI, H</creatorcontrib><creatorcontrib>FUKUYAMA, H</creatorcontrib><creatorcontrib>NAGAHAMA, Y</creatorcontrib><creatorcontrib>KATSUMI, Y</creatorcontrib><creatorcontrib>OKAZAWA, H</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>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Stroke (1970)</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>YAMAUCHI, H</au><au>FUKUYAMA, H</au><au>NAGAHAMA, Y</au><au>KATSUMI, Y</au><au>OKAZAWA, H</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cerebral hematocrit decreases with hemodynamic compromise in carotid artery occlusion : A PET study</atitle><jtitle>Stroke (1970)</jtitle><addtitle>Stroke</addtitle><date>1998</date><risdate>1998</risdate><volume>29</volume><issue>1</issue><spage>98</spage><epage>103</epage><pages>98-103</pages><issn>0039-2499</issn><eissn>1524-4628</eissn><coden>SJCCA7</coden><abstract>This study investigated whether in patients with internal carotid artery occlusion the regional cerebral hematocrit correlates with cerebral hemodynamics or metabolic state and, if so, how the regional cerebral hematocrit changes in the hemodynamically compromised region.
We used positron emission tomography to study seven patients with unilateral internal carotid artery occlusion and no cortical infarction in the chronic stage. The distributions of red blood cell and plasma volumes were assessed using oxygen-15-labeled carbon monoxide and copper-62-labeled human serum albumin-dithiosemicarbazone tracers, respectively. The calculated hematocrit value was compared with the hemodynamic and metabolic parameters measured with the oxygen-15 steady-state technique.
In the cerebral cortex, the value of the cerebral hematocrit varied but was correlated with the hemodynamic and metabolic status. Stepwise regression analysis revealed that the large vessel hematocrit, the cerebral metabolic rate of oxygen, and the cerebral blood flow or the oxygen extraction fraction accounted for a significant proportion of variance of the cerebral hematocrit. The oxygen extraction fraction and the cerebral metabolic rate of oxygen negatively correlated with the cerebral hematocrit, whereas the cerebral blood flow correlated positively: patients with reduced blood supply relative to metabolic demand (decreased blood flow with increased oxygen extraction fraction) showed low hematocrit values.
In carotid artery occlusion in the chronic stage, regional cerebral hematocrit may vary according to cerebral hemodynamics and metabolic status. Regional cerebral hematocrit may decrease with hemodynamic compromise unless oxygen metabolism concomitantly decreases.</abstract><cop>Hagerstown, MD</cop><pub>Lippincott Williams & Wilkins</pub><pmid>9445336</pmid><doi>10.1161/01.STR.29.1.98</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
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| source | MEDLINE; American Heart Association Journals; Journals@Ovid Complete; EZB-FREE-00999 freely available EZB journals; Alma/SFX Local Collection |
| subjects | Aged Biological and medical sciences Brain - diagnostic imaging Brain - metabolism Brain - physiopathology Brain Ischemia - blood Brain Ischemia - diagnostic imaging Brain Ischemia - physiopathology Carbon Monoxide Carotid Artery Diseases - blood Carotid Artery Diseases - diagnostic imaging Carotid Artery Diseases - physiopathology Carotid Artery, Internal - diagnostic imaging Carotid Artery, Internal - physiopathology Cerebral Cortex - diagnostic imaging Cerebral Cortex - metabolism Cerebral Cortex - physiopathology Cerebral Infarction - blood Cerebral Infarction - diagnostic imaging Cerebral Infarction - physiopathology Cerebrovascular Circulation - physiology Chronic Disease Copper Radioisotopes Female Hematocrit Hemodynamics Humans Male Medical sciences Middle Aged Neurology Oxygen Consumption - physiology Oxygen Radioisotopes Plasma Volume Radiopharmaceuticals Regression Analysis Serum Albumin Thiosemicarbazones Tomography, Emission-Computed Vascular diseases and vascular malformations of the nervous system |
| title | Cerebral hematocrit decreases with hemodynamic compromise in carotid artery occlusion : A PET study |
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