AJP - Regu Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Regul Integr Comp Physiol 257: R1265-R1281, 1989;
0363-6119/89 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Right arrow Citation Map
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Abel, F. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Abel, F. L.

AJP - Regulatory, Integrative and Comparative Physiology, Vol 257, Issue 6 1265-R1281, Copyright © 1989 by American Physiological Society

ARTICLES

Myocardial function in sepsis and endotoxin shock

F. L. Abel
Department of Physiology, University of South Carolina School of Medicine, Columbia 29208.

Myocardial function in sepsis and endotoxin shock is reviewed. Clinical, whole animal, and isolated tissue studies are compared to answer the question whether sepsis and/or endotoxin directly damage the myocardium. Myocardial performance is considered relative to control of preload, afterload, and heart rate. Despite the fact that these vary widely in different studies, there is overwhelming evidence that myocardial performance is depressed in both sepsis and endotoxin shock. The depression is dose related, occurs early after large doses of endotoxin but may follow a hyperdynamic phase in sepsis or after low doses of endotoxin. Endotoxin itself does not appear to be the depressant factor; the final depressant substance(s) is unknown. Calcium transport by the sarcoplasmic reticulum is depressed. This defect is more prominent in the endocardium than in the epicardium. Myocardial adenosinetriphosphatase (ATPase) and norepinephrine stores may be depleted. The septic myocardium has an increased dependence on sympathetic nerve stimulation. There is little evidence that the cause of the myocardial depression is an inadequate coronary blood flow.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Cell Physiol.Home page
A. K. Grover, C.-Y. Kwan, and S. E. Samson
Effects of peroxynitrite on sarco/endoplasmic reticulum Ca2+ pump isoforms SERCA2b and SERCA3a
Am J Physiol Cell Physiol, December 1, 2003; 285(6): C1537 - C1543.
[Abstract] [Full Text] [PDF]

Home page
 Br J AnaesthHome page
R. Serita, H. Morisaki, K. Ai, Y. Morita, Y. Innami, T. Satoh, S. Kosugi, Y. Kotake, and J. Takeda
Sevoflurane preconditions stunned myocardium in septic but not healthy isolated rat hearts
Br. J. Anaesth., December 1, 2002; 89(6): 896 - 903.
[Abstract] [Full Text] [PDF]

Home page
 ChestHome page
F. Jardin, T. Fourme, B. Page, Y. Loubieres, A. Vieillard-Baron, A. Beauchet, and J.-P. Bourdarias
Persistent Preload Defect in Severe Sepsis Despite Fluid Loading: A Longitudinal Echocardiographic Study in Patients With Septic Shock
Chest, November 1, 1999; 116(5): 1354 - 1359.
[Abstract] [Full Text] [PDF]

Home page
 Am. J. Respir. Crit. Care Med.Home page
A. KOVACS, M. R. COURTOIS, B. BARZILAI, I. E. KARL, P. A. LUDBROOK, and R. S. HOTCHKISS
Reversal of Hypocalcemia and Decreased Afterload in Sepsis . Effect on Myocardial Systolic and Diastolic Function
Am. J. Respir. Crit. Care Med., December 1, 1998; 158(6): 1990 - 1998.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
S. Sakurada and J. R. S. Hales
A role for gastrointestinal endotoxins in enhancement of heat tolerance by physical fitness
J Appl Physiol, January 1, 1998; 84(1): 207 - 214.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online