title: Biphasic changes in left ventricular function during hyperdynamic endotoxemia.
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 (EES)] 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 micrograms . kg-1. h-1) was administered intravenously for 24 h. EES 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. EES decreased in the later phase. A similar biphasic response of EES has been reported during a tumor necrosis factor-alpha (TNF) challenge. Even though plasma TNF was highest at 1 h and declined thereafter in this study, no consistent relationship between TNF and EES was identified, and TNF levels did not correlate directly with the changes in EES.
authors.affiliation: United States Army Institute of Surgical Research, Fort Sam Houston, Texas 78234, USA.
authors.forename: S
authors.initials: S
authors.lastname: Ishihara
authors.forename: J A
authors.initials: JA
authors.lastname: Ward
authors.forename: O
authors.initials: O
authors.lastname: Tasaki
authors.forename: B A
authors.initials: BA
authors.lastname: Pruitt
authors.forename: M A
authors.initials: MA
authors.lastname: Javors
authors.forename: R A
authors.initials: RA
authors.lastname: Cassidy
authors.forename: D W
authors.initials: DW
authors.lastname: Mozingo
mesh_terms: D000818:Animals; D001794:Blood Pressure / Q000502:physiology; D019446:Endotoxemia / Q000503:physiopathology*; D004731:Endotoxins; D005260:Female; D006339:Heart Rate / Q000502:physiology; D009200:Myocardial Contraction / Q000502:physiology; D018805:Sepsis / Q000503:physiopathology; D013318:Stroke Volume / Q000502:physiology; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D004731:Endotoxins; D014409:Tumor Necrosis Factor-alpha