Advertisement

Amendment history:

Research Article Free access | 10.1172/JCI113866

Role of endotoxemia in cardiovascular dysfunction and mortality. Escherichia coli and Staphylococcus aureus challenges in a canine model of human septic shock.

C Natanson, R L Danner, R J Elin, J M Hosseini, K W Peart, S M Banks, T J MacVittie, R I Walker, and J E Parrillo

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Natanson, C. in: JCI | PubMed | Google Scholar

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Danner, R. in: JCI | PubMed | Google Scholar

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Elin, R. in: JCI | PubMed | Google Scholar

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Hosseini, J. in: JCI | PubMed | Google Scholar

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Peart, K. in: JCI | PubMed | Google Scholar

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Banks, S. in: JCI | PubMed | Google Scholar

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by MacVittie, T. in: JCI | PubMed | Google Scholar

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Walker, R. in: JCI | PubMed | Google Scholar

Critical Care Medicine Department, National Institutes of Health, Bethesda, Maryland 20892.

Find articles by Parrillo, J. in: JCI | PubMed | Google Scholar

Published January 1, 1989 - More info

Published in Volume 83, Issue 1 on January 1, 1989
J Clin Invest. 1989;83(1):243–251. https://doi.org/10.1172/JCI113866.
© 1989 The American Society for Clinical Investigation
Published January 1, 1989 - Version history
View PDF
Abstract

Using different types of bacteria and a canine model simulating human septic shock, we investigated the role of endotoxin in cardiovascular dysfunction and mortality. Either Escherichia coli (a microorganism with endotoxin) or Staphylococcus aureus (a microorganism without endotoxin) were placed in an intraperitoneal clot in doses of viable or formalin-killed bacteria. Cardiovascular function of conscious animals was studied using simultaneous radionuclide heart scans and thermodilution cardiac outputs. Serial plasma endotoxin levels were measured. S. aureus produced a pattern of reversible cardiovascular dysfunction over 7-10 d that was concordant (P less than 0.01) with that of E. coli. Although this cardiovascular pattern was not altered by formalin killing (S. aureus and E. coli), formalin-killed organisms produced a lower mortality and less myocardial depression (P less than 0.01). S. aureus, compared to E. coli, produced higher postmortem concentrations of microorganisms and higher mortality (P less than 0.025). E. coli produced significant endotoxemia (P less than 0.01), though viable organisms (versus nonviable) resulted in higher endotoxin blood concentrations (P less than 0.05). Significant endotoxemia did not occur with S. aureus. Thus, in the absence of endotoxemia, S. aureus induced the same cardiovascular abnormalities of septic shock as E. coli. These findings indicate that structurally and functionally distinct microorganisms, with or without endotoxin, can activate a common pathway resulting in similar cardiovascular injury and mortality.

Browse pages

Click on an image below to see the page. View PDF of the complete article

Version history
  • Version 1 (January 1, 1989): No description
Advertisement
Advertisement