Document Detail


Anti-tumor necrosis factor-alpha prevents decreased ventricular contractility in endotoxemic pigs.
MedLine Citation:
PMID:  7633696     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
It is not known how the decrease in left ventricular contractility following endotoxin exposure is mediated, or whether this decrease is preventable by antibodies to tumor necrosis factor-alpha (TNF alpha). Four groups of six anesthetized and instrumented pigs were pretreated with ovine polyclonal antibody to human TNF alpha (anti-TNF alpha), nonspecific IgG, or saline, and then treated with either endotoxin or saline. We measured hemodynamics and left ventricular pressures (Millar catheter) and volumes (conductance catheter). Left ventricular contractility was assessed using the slope (Emax) of the end-systolic pressure-volume relationship. Four hours after the start of endotoxin infusion in the nonspecific IgG pretreated group, Emax had decreased by 44 +/- 6% (p < 0.05), mean arterial pressure had decreased from 115 +/- 7 mm Hg to 70 +/- 10 mm Hg (p < 0.05), and cardiac output was rapidly decreasing after an initial increase (p < 0.05). Anti-TNF alpha significantly reduced the decrease in Emax (11 +/- 9%, p < 0.05), and the systemic hypotension (108 +/- 15 mm Hg to 99 +/- 6 mm Hg, p < 0.05), at 4 h, and prevented the late decrease in cardiac output. This suggests that TNF alpha is an important early mediator in sepsis leading to decreased left ventricular contractility.
Authors:
M J Herbertson; H A Werner; C M Goddard; J A Russell; A Wheeler; R Coxon; K R Walley
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  American journal of respiratory and critical care medicine     Volume:  152     ISSN:  1073-449X     ISO Abbreviation:  Am. J. Respir. Crit. Care Med.     Publication Date:  1995 Aug 
Date Detail:
Created Date:  1995-09-14     Completed Date:  1995-09-14     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  9421642     Medline TA:  Am J Respir Crit Care Med     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  480-8     Citation Subset:  AIM; IM    
Affiliation:
Pulmonary Research Laboratory, St. Paul's Hospital, University of British Columbia, Vancouver, Canada.
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MeSH Terms
Descriptor/Qualifier:
Animals
Antibodies / immunology*
Atrial Function, Right / immunology
Blood Pressure / immunology
Cardiac Output / immunology
Cardiac Volume / immunology
Endotoxins / blood*,  immunology
Heart Rate / immunology
Humans
Immunoglobulin G / immunology
Myocardial Contraction / immunology*
Pulmonary Artery
Sheep
Shock, Septic / immunology*
Stroke Volume / immunology
Swine
Systole
Tumor Necrosis Factor-alpha / immunology*
Vascular Resistance / immunology
Ventricular Function, Left / immunology*
Ventricular Pressure / immunology
Chemical
Reg. No./Substance:
0/Antibodies; 0/Endotoxins; 0/Immunoglobulin G; 0/Tumor Necrosis Factor-alpha

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


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