Document Detail

Acetate fails to reverse myocardial depression in dogs anesthetized with halothane.
MedLine Citation:
PMID:  568399     Owner:  NLM     Status:  MEDLINE    
Sodium acetate has been shown to reverse the myocardial depression induced by halothane in vitro. The biochemical basis for this restoration of contractility has been located in the glycolytic pathway. The present study was designed to determine whether this antagonistic property of acetate also occurs in vivo. Dogs autonomically blocked with guanethidine, phenoxybenzamine, and atropine were sequentially anesthetized with halothane in O2 and N2O-O2-succinylcholine in a random pattern. All animals were given sodium acetate IV in amounts adequate to produce pharmacologically active levels. Myocardial performance was measured by LVdP/dtmax, LVPDP/dt/KPmax, and Vmax. Halothane effected a significant depression of these myocardial parameters. Acetate did not reverse this depressant effect of halothane. Acetate, a well-established peripheral vascular vasodilator, did decrease left ventricular and aortic pressures.
S H Jackson; N T Smith
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Anesthesia and analgesia     Volume:  57     ISSN:  0003-2999     ISO Abbreviation:  Anesth. Analg.     Publication Date:    1978 Jul-Aug
Date Detail:
Created Date:  1978-12-20     Completed Date:  1978-12-20     Revised Date:  2003-11-14    
Medline Journal Info:
Nlm Unique ID:  1310650     Medline TA:  Anesth Analg     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  395-403     Citation Subset:  AIM; IM    
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MeSH Terms
Acetates / blood,  pharmacology*
Anesthesia, Inhalation*
Atropine / pharmacology
Blood Chemical Analysis
Blood Pressure / drug effects
Guanethidine / pharmacology
Halothane / antagonists & inhibitors*,  pharmacology
Heart / drug effects*
Phenoxybenzamine / pharmacology
Reg. No./Substance:
0/Acetates; 151-67-7/Halothane; 51-55-8/Atropine; 55-65-2/Guanethidine; 59-96-1/Phenoxybenzamine

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

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