| Metoprolol reduces cerebral tissue oxygen tension after acute hemodilution in rats. | |
| | |
MedLine Citation:
|
PMID: 19809291 Owner: NLM Status: MEDLINE |
Abstract/OtherAbstract:
|
BACKGROUND: Perioperative beta-blockade and anemia are independent predictors of increased stroke and mortality by undefined mechanisms. This study investigated the effect of beta-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 x kg) or saline before undergoing hemodilution with pentastarch (1:1 blood volume exchange, 30 ml x kg). Outcomes included cardiac output, cerebral blood flow, and brain (PBrO2) and kidney (PKO2) tissue oxygen tension. Hypoxia inducible factor-1alpha (HIF-1alpha) 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). Beta-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-1alpha protein levels were increased in beta-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 beta-blockade and hemodilution. CONCLUSIONS: Cerebral tissue oxygen tension is preferentially maintained during hemodilution, relative to the kidney, despite elevated systemic catecholamines. Acute beta-blockade impaired the compensatory cardiac output response to hemodilution, resulting in a reduction in cerebral tissue oxygen tension and increased expression of HIF-1alpha. |
| | |
Authors:
|
Tenille E Ragoonanan; W Scott Beattie; C David Mazer; Albert K Y Tsui; Howard Leong-Poi; David F Wilson; Gordon Tait; Julie Yu; Elaine Liu; Melissa Noronha; Neil D Dattani; Nicholas Mitsakakis; Gregory M T Hare |
Publication Detail:
|
Type: Journal Article; Research Support, N.I.H., Extramural; Research Support, Non-U.S. Gov't |
Journal Detail:
|
Title: Anesthesiology Volume: 111 ISSN: 1528-1175 ISO Abbreviation: Anesthesiology Publication Date: 2009 Nov |
Date Detail:
|
Created Date: 2009-10-28 Completed Date: 2009-11-13 Revised Date: - |
Medline Journal Info:
|
Nlm Unique ID: 1300217 Medline TA: Anesthesiology Country: United States |
Other Details:
|
Languages: eng Pagination: 988-1000 Citation Subset: AIM; IM |
Affiliation:
|
Department of Anesthesia, Keenan Research Centre of the Li Ka Shing Knowledge Institute, St. Michael's Hospital, University of Toronto, Toronto, Ontario, Canada. |
Export Citation:
|
APA/MLA Format Download EndNote Download BibTex |
| MeSH Terms | |
Descriptor/Qualifier:
|
Adrenergic beta-Antagonists
/
pharmacology* Angiotensin II / blood Animals Brain / drug effects*, metabolism Cardiac Output / drug effects Catecholamines / blood Cerebrovascular Circulation / drug effects Erythropoietin / blood Hemodilution* Hypoxia-Inducible Factor 1, alpha Subunit / analysis Male Metoprolol / adverse effects, pharmacology* Oxygen / metabolism* Rats Rats, Sprague-Dawley Stroke / etiology |
| Grant Support | |
ID/Acronym/Agency:
|
NS-31465/NS/NINDS NIH HHS |
| Chemical | |
Reg. No./Substance:
|
0/Adrenergic beta-Antagonists; 0/Catecholamines; 0/Hif1a protein, rat; 0/Hypoxia-Inducible Factor 1, alpha Subunit; 11096-26-7/Erythropoietin; 11128-99-7/Angiotensin II; 37350-58-6/Metoprolol; 7782-44-7/Oxygen |
From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine
Previous Document: Should anesthesia groups advocate funding of clinics and scheduling systems to increase operating ro...
Next Document: Prevention of Atelectasis in Morbidly Obese Patients during General Anesthesia and Paralysis: A Comp...