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- Publisher Website: 10.1097/ALN.0b013e3181b87f0e
- Scopus: eid_2-s2.0-70449585638
- PMID: 19809291
- WOS: WOS:000271172500010
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Article: Metoprolol reduces cerebral tissue oxygen tension after acute hemodilution in rats
Title | Metoprolol reduces cerebral tissue oxygen tension after acute hemodilution in rats |
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Authors | |
Issue Date | 2009 |
Citation | Anesthesiology, 2009, v. 111, n. 5, p. 988-1000 How to Cite? |
Abstract | BACKGROUND:: Perioperative β-blockade and anemia are independent predictors of increased stroke and mortality by undefined mechanisms. This study investigated the effect of β-blockade on cerebral tissue oxygen delivery in an experimental model of blood loss and fluid resuscitation (hemodilution). METHODS:: Anesthetized rats were treated with metoprolol (3 mg • kg) or saline before undergoing hemodilution with pentastarch (1:1 blood volume exchange, 30 ml • kg). Outcomes included cardiac output, cerebral blood flow, and brain (PBrO2) and kidney (PKO2) tissue oxygen tension. Hypoxia inducible factor-1α (HIF-1α) protein levels were assessed by Western blot. Systemic catecholamines, erythropoietin, and angiotensin II levels were measured. RESULTS:: Hemodilution increased heart rate, stroke volume, cardiac output (60%), and cerebral blood flow (50%), thereby maintaining PBrO2 despite an approximately 50% reduction in blood oxygen content (P < 0.05 for all). By contrast, PKO2 decreased (50%) under the same conditions (P < 0.05). β-blockade reduced baseline heart rate (20%) and abolished the compensatory increase in cardiac output after hemodilution (P < 0.05). This attenuated the cerebral blood flow response and reduced PBrO2 (50%), without further decreasing PKO2. Cerebral HIF-1α protein levels were increased in β-blocked hemodiluted rats relative to hemodiluted controls (P < 0.05). Systemic catecholamine and erythropoietin levels increased comparably after hemodilution in both groups, whereas angiotensin II levels increased only after β-blockade and hemodilution. CONCLUSIONS:: Cerebral tissue oxygen tension is preferentially maintained during hemodilution, relative to the kidney, despite elevated systemic catecholamines. Acute β-blockade impaired the compensatory cardiac output response to hemodilution, resulting in a reduction in cerebral tissue oxygen tension and increased expression of HIF-1α. © 2009 the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. |
Persistent Identifier | http://hdl.handle.net/10722/205729 |
ISSN | 2021 Impact Factor: 8.986 2020 SCImago Journal Rankings: 1.874 |
ISI Accession Number ID |
DC Field | Value | Language |
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dc.contributor.author | Ragoonanan, Tenille E. | - |
dc.contributor.author | Beattie, William Scott | - |
dc.contributor.author | Mazer, Cynthia David | - |
dc.contributor.author | Tsui, Albert K Y | - |
dc.contributor.author | Leong-Poi, Howard | - |
dc.contributor.author | Wilson, David F. | - |
dc.contributor.author | Tait, Gordon A. | - |
dc.contributor.author | Yu, Julie | - |
dc.contributor.author | Liu, Elaine | - |
dc.contributor.author | Noronha, Melissa | - |
dc.contributor.author | Dattani, Neil D. | - |
dc.contributor.author | Mitsakakis, Nicholas | - |
dc.contributor.author | Haré, Gregory M T | - |
dc.date.accessioned | 2014-10-06T08:02:16Z | - |
dc.date.available | 2014-10-06T08:02:16Z | - |
dc.date.issued | 2009 | - |
dc.identifier.citation | Anesthesiology, 2009, v. 111, n. 5, p. 988-1000 | - |
dc.identifier.issn | 0003-3022 | - |
dc.identifier.uri | http://hdl.handle.net/10722/205729 | - |
dc.description.abstract | BACKGROUND:: Perioperative β-blockade and anemia are independent predictors of increased stroke and mortality by undefined mechanisms. This study investigated the effect of β-blockade on cerebral tissue oxygen delivery in an experimental model of blood loss and fluid resuscitation (hemodilution). METHODS:: Anesthetized rats were treated with metoprolol (3 mg • kg) or saline before undergoing hemodilution with pentastarch (1:1 blood volume exchange, 30 ml • kg). Outcomes included cardiac output, cerebral blood flow, and brain (PBrO2) and kidney (PKO2) tissue oxygen tension. Hypoxia inducible factor-1α (HIF-1α) protein levels were assessed by Western blot. Systemic catecholamines, erythropoietin, and angiotensin II levels were measured. RESULTS:: Hemodilution increased heart rate, stroke volume, cardiac output (60%), and cerebral blood flow (50%), thereby maintaining PBrO2 despite an approximately 50% reduction in blood oxygen content (P < 0.05 for all). By contrast, PKO2 decreased (50%) under the same conditions (P < 0.05). β-blockade reduced baseline heart rate (20%) and abolished the compensatory increase in cardiac output after hemodilution (P < 0.05). This attenuated the cerebral blood flow response and reduced PBrO2 (50%), without further decreasing PKO2. Cerebral HIF-1α protein levels were increased in β-blocked hemodiluted rats relative to hemodiluted controls (P < 0.05). Systemic catecholamine and erythropoietin levels increased comparably after hemodilution in both groups, whereas angiotensin II levels increased only after β-blockade and hemodilution. CONCLUSIONS:: Cerebral tissue oxygen tension is preferentially maintained during hemodilution, relative to the kidney, despite elevated systemic catecholamines. Acute β-blockade impaired the compensatory cardiac output response to hemodilution, resulting in a reduction in cerebral tissue oxygen tension and increased expression of HIF-1α. © 2009 the American Society of Anesthesiologists, Inc. Lippincott Williams & Wilkins, Inc. | - |
dc.language | eng | - |
dc.relation.ispartof | Anesthesiology | - |
dc.title | Metoprolol reduces cerebral tissue oxygen tension after acute hemodilution in rats | - |
dc.type | Article | - |
dc.description.nature | link_to_subscribed_fulltext | - |
dc.identifier.doi | 10.1097/ALN.0b013e3181b87f0e | - |
dc.identifier.pmid | 19809291 | - |
dc.identifier.scopus | eid_2-s2.0-70449585638 | - |
dc.identifier.volume | 111 | - |
dc.identifier.issue | 5 | - |
dc.identifier.spage | 988 | - |
dc.identifier.epage | 1000 | - |
dc.identifier.eissn | 1528-1175 | - |
dc.identifier.isi | WOS:000271172500010 | - |
dc.identifier.issnl | 0003-3022 | - |