Biphasic changes in left ventricular function during hyperdynamic endotoxemia

Satoshi Ishihara, John A. Ward, Osamu Tasaki, Basil A. Pruitt, Martine A. Javors, Richard A. Cassidy, David W. Mozingo

Research output: Contribution to journalArticle

10 Scopus citations

Abstract

Cardiac contractility was studied in a clinically relevant conscious swine model simulating human hemodynamics during endotoxemia. The slope of the end-systolic pressure-volume relationship [end-systolic elastance (E(ES))] was used as a load-independent contractility index. Chronic instrumentation in 10 pigs included two pairs of endocardial ultrasonic crystals for measuring internal major and minor axial dimensions of the left ventricle, a micromanometer for left ventricular pressure measurement, and a thermodilution pulmonary artery catheter. After a 10-day recovery period, control measurements of cardiac hemodynamic function were obtained. The following week, Escherichia coli endotoxin (10 μg · kg-1 · h-1) was administered intravenously for 24 h. E(ES) increased 1 h after endotoxin infusion and decreased beyond 7 h. The later hemodynamic changes resembled human cardiovascular performance during endotoxemia more closely than the changes during the acute phase. E(ES) decreased in the later phase. A similar biphasic response of E(ES) has been reported during a tumor necrosis factor- α (TNF) challenge. Even though plasma TNF was highest at I h and declined thereafter in this study, no consistent relationship between TNF and E(ES) was identified, and TNF levels did not correlate directly with the changes in E(ES).

Original languageEnglish (US)
Pages (from-to)R1516-R1524
JournalAmerican Journal of Physiology - Regulatory Integrative and Comparative Physiology
Volume276
Issue number5 45-5
DOIs
StatePublished - May 1999

Keywords

  • Contractility
  • Endotoxin
  • Hemodynamics
  • Left ventricle
  • Tumor necrosis factor-α

ASJC Scopus subject areas

  • Physiology
  • Physiology (medical)

Fingerprint Dive into the research topics of 'Biphasic changes in left ventricular function during hyperdynamic endotoxemia'. Together they form a unique fingerprint.

  • Cite this