Source:http://linkedlifedata.com/resource/pubmed/id/11429359
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
1
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pubmed:dateCreated |
2001-6-28
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pubmed:abstractText |
We compared sodium nitroprusside (SNP)-induced hypotension with 3% isoflurane-induced hypotension with regard to brain tissue oxygen pressure (PtO(2)), middle cerebral artery (MCA) blood flow, and cerebral arteriovenous shunting. Eight dogs were anesthetized with 1.5% isoflurane. After a craniotomy, a probe was inserted into the left frontoparietal brain cortex to mea-sure tissue gases and pH. Blood flow was measured in a secondary branch of the MCA by a flowprobe. Measurements were made during baseline 1.5% isoflurane, during 1.5% isoflurane and SNP-induced hypotension or 3% isoflurane-induced hypotension to a mean pressure of 60-65 mm Hg, and during continued treatment with SNP or 3% isoflurane with blood pressure support to baseline levels with phenylephrine. Shunting was calculated from arterial, sagittal sinus, and tissue (indicating capillary) oxygen content. During hypotension with SNP, PtO(2) decreased 50%, and shunting increased 50%. During hypotension with 3% isoflurane, PtO(2) and shunting did not change. Blood pressure support increased PtO(2) and MCA flow during both SNP and 3% isoflurane treatment. These results show that SNP is a cerebrovasodilator but that hypotension will decrease PtO(2), probably because of an increase in arteriovenous shunting and a decrease in capillary perfusion. Implications: We measured brain arteriovenous shunting and tissue oxygen pressure(PtO(2))during a 40% decrease in blood pressure induced by sodium nitroprusside (SNP)or 3% isoflurane. Large-dose isoflurane maintainedPtO(2) with no change in shunting. SNP infusion decreasedPtO(2) 50%and increased shunting 50%. This suggests that SNP-induced hypotension decreases PtO(2) because of a decrease in capillary perfusion.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Jul
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pubmed:issn |
0003-2999
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
93
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
166-70
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pubmed:dateRevised |
2007-11-15
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pubmed:meshHeading |
pubmed-meshheading:11429359-Anesthetics, Inhalation,
pubmed-meshheading:11429359-Animals,
pubmed-meshheading:11429359-Antihypertensive Agents,
pubmed-meshheading:11429359-Arteriovenous Fistula,
pubmed-meshheading:11429359-Blood Gas Analysis,
pubmed-meshheading:11429359-Body Temperature,
pubmed-meshheading:11429359-Brain Chemistry,
pubmed-meshheading:11429359-Cerebrovascular Circulation,
pubmed-meshheading:11429359-Dogs,
pubmed-meshheading:11429359-Hemodynamics,
pubmed-meshheading:11429359-Hydrogen-Ion Concentration,
pubmed-meshheading:11429359-Hypotension,
pubmed-meshheading:11429359-Isoflurane,
pubmed-meshheading:11429359-Middle Cerebral Artery,
pubmed-meshheading:11429359-Nitroprusside,
pubmed-meshheading:11429359-Oxygen Consumption
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pubmed:year |
2001
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pubmed:articleTitle |
Sodium nitroprusside compared with isoflurane-induced hypotension: the effects on brain oxygenation and arteriovenous shunting.
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pubmed:affiliation |
Department of Anesthesiology, University of Illinois at Chicago, 60612, USA. whoffman@uic.edu
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pubmed:publicationType |
Journal Article,
Comparative Study
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