Document Detail

Endotoxin impairs cardiac hemodynamics by affecting loading conditions but not by reducing cardiac inotropism.
MedLine Citation:
PMID:  20525873     Owner:  NLM     Status:  MEDLINE    
Acute myocardial dysfunction is a typical manifestation of septic shock. Experimentally, the administration of endotoxin [lipopolysacharride (LPS)] to laboratory animals is frequently used to study such dysfunction. However, a majority of studies used load-dependent indexes of cardiac function [including ejection fraction (EF) and maximal systolic pressure increment (dP/dt(max))], which do not directly explore cardiac inotropism. Therefore, we evaluated the direct effects of LPS on myocardial contractility, using left ventricular (LV) pressure-volume catheters in mice. Male BALB/c mice received an intraperitoneal injection of E. coli LPS (1, 5, 10, or 20 mg/kg). After 2, 6, or 20 h, cardiac function was analyzed in anesthetized, mechanically ventilated mice. All doses of LPS induced a significant drop in LV stroke volume and a trend toward reduced cardiac output after 6 h. Concomitantly, there was a significant decrease of LV preload (LV end-diastolic volume), with no apparent change in LV afterload (evaluated by effective arterial elastance and systemic vascular resistance). Load-dependent indexes of LV function were markedly reduced at 6 h, including EF, stroke work, and dP/dt(max). In contrast, there was no reduction of load-independent indexes of LV contractility, including end-systolic elastance (ejection phase measure of contractility) and the ratio dP/dt(max)/end-diastolic volume (isovolumic phase measure of contractility), the latter showing instead a significant increase after 6 h. All changes were transient, returning to baseline values after 20 h. Therefore, the alterations of cardiac function induced by LPS are entirely due to altered loading conditions, but not to reduced contractility, which may instead be slightly increased.
Li Jianhui; Nathalie Rosenblatt-Velin; Noureddine Loukili; Pal Pacher; François Feihl; Bernard Waeber; Lucas Liaudet
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-06-04
Journal Detail:
Title:  American journal of physiology. Heart and circulatory physiology     Volume:  299     ISSN:  1522-1539     ISO Abbreviation:  Am. J. Physiol. Heart Circ. Physiol.     Publication Date:  2010 Aug 
Date Detail:
Created Date:  2010-07-30     Completed Date:  2010-08-30     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  100901228     Medline TA:  Am J Physiol Heart Circ Physiol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  H492-501     Citation Subset:  IM    
Dept. of Intensive Care Medicine, Univ. Hospital Center and Faculty of Biology and Medicine, CHUV-BH 08-621, 1011 Lausanne, Switzerland.
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MeSH Terms
Arteries / physiopathology
Cardiac Catheterization
Cardiomyopathies / etiology*,  physiopathology
Disease Models, Animal
Dose-Response Relationship, Drug
Endotoxemia / chemically induced,  complications*,  physiopathology
Endotoxins / administration & dosage
Heart Rate
Injections, Intraperitoneal
Mice, Inbred BALB C
Models, Cardiovascular
Myocardial Contraction*
Stroke Volume
Time Factors
Vascular Resistance
Ventricular Function, Left*
Ventricular Pressure
Reg. No./Substance:
0/Endotoxins; 67924-63-4/endotoxin, Escherichia coli

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