Document Detail


Lipid infusion accelerates removal of bupivacaine and recovery from bupivacaine toxicity in the isolated rat heart.
MedLine Citation:
PMID:  16857549     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
BACKGROUND AND OBJECTIVES: Infusion of a lipid emulsion has been advocated for treatment of severe bupivacaine cardiac toxicity. The mechanism of lipid rescue is unknown. These studies address the possibility that lipid infusion reduces cardiac bupivacaine content in the context of cardiac toxicity. METHODS: We compared the effects of a 1% lipid emulsion with standard Krebs buffer after inducing asystole in isolated rat heart with 500 micromol/L bupivacaine. We compared times to first heart beat and recovery of 90% of baseline rate pressure product (RPP = heart rate x [left ventricular systolic pressure - left ventricular diastolic pressure]) between controls and hearts receiving 1% lipid immediately after bupivacaine. We also used minibiopsies to compare control bupivacaine tissue content with hearts getting lipid immediately after an infusion of radiolabeled bupivacaine. We then compared bupivacaine efflux from hearts with and without lipid infusion started 75 seconds after radiolabeled bupivacaine was administered. RESULTS: Infusion of lipid resulted in more rapid return of spontaneous contractions and full recovery of cardiac function. Average (+/- SEM) times to first beat and to 90% recovery of rate pressure product were 44.6 +/- 3.5 versus 63.8 +/- 4.3 seconds (P < .01) and 124.7 +/- 12.4 versus 219.8 +/- 25.6 seconds (P < .01) for lipid and controls, respectively. Lipid treatment resulted in more rapid loss of bupivacaine from heart tissue (P < .0016). Late lipid infusion, 75 seconds after bupivacaine infusion ended, increased the release of bupivacaine measured in effluent for the first 15-second interval compared with controls (183 vs. 121 nmol, n = 5 for both groups, P < .008). CONCLUSIONS: Lipid emulsion speeds loss of bupivacaine from cardiac tissue while accelerating recovery from bupivacaine-induced asystole. These findings are consistent with the hypothesis that bupivacaine partitions into the emulsion and supports the concept of a "lipid sink." However, the data do not exclude other possible mechanisms of action.
Authors:
Guy L Weinberg; Richard Ripper; Patricia Murphy; Lucas B Edelman; William Hoffman; Gary Strichartz; Douglas L Feinstein
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Regional anesthesia and pain medicine     Volume:  31     ISSN:  1098-7339     ISO Abbreviation:  Reg Anesth Pain Med     Publication Date:    2006 Jul-Aug
Date Detail:
Created Date:  2006-07-21     Completed Date:  2006-09-12     Revised Date:  2009-07-10    
Medline Journal Info:
Nlm Unique ID:  9804508     Medline TA:  Reg Anesth Pain Med     Country:  United States    
Other Details:
Languages:  eng     Pagination:  296-303     Citation Subset:  IM    
Affiliation:
Department of Anesthesiology, University of Illinois College of Medicine at Chicago, Chicago, IL 60612, USA. guyw@uic.edu
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MeSH Terms
Descriptor/Qualifier:
Analysis of Variance
Anesthetics, Local / metabolism,  toxicity
Animals
Biopsy
Blood Pressure / drug effects
Bupivacaine / metabolism*,  toxicity*
Fat Emulsions, Intravenous / administration & dosage,  pharmacology*
Heart / drug effects*
Heart Rate / drug effects
Infusions, Intravenous / methods
Male
Myocardium / metabolism*
Rats
Rats, Sprague-Dawley
Time Factors
Chemical
Reg. No./Substance:
0/Anesthetics, Local; 0/Fat Emulsions, Intravenous; 2180-92-9/Bupivacaine
Comments/Corrections
Comment In:
Reg Anesth Pain Med. 2009 May-Jun;34(3):276   [PMID:  19436187 ]
Reg Anesth Pain Med. 2007 May-Jun;32(3):270-1; author reply 271   [PMID:  17543829 ]

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine


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