title: Mechanoenergetic inefficiency in the septic left ventricle is due to enhanced oxygen requirements for excitation-contraction coupling.
abstract: OBJECTIVE
  Myocardial oxygen consumption (MVO2) in the septic myocardium is increased despite reduced left ventricular mechanical work. We investigated the mechanism behind this energetic inefficiency in the septic myocardium.
  
  
  METHODS
  To clarify whether energy consumption in basal metabolism or excitation-contraction (EC) coupling is elevated in the septic myocardium, we separated MVO2 used for these two processes. We assessed hemodynamics, left ventricular pressure-volume area, left ventricular MVO2, myocardial substrate metabolism and the inflammatory response in eight control pigs and in eight septic pigs receiving E. coli endotoxin. Using cardiopulmonary bypass (CPB), unloaded MVO2 was assessed before and after arrest of electromechanical activity using KCl infusions.
  
  
  RESULTS
  Unloaded MVO2 was significantly higher in the septic group compared to the control group (65.7 +/- 12.9 vs. 43.3 +/- 15.1 J.min(-1).100 g LV(-1), p < 0.005), but basal MVO2 after 5 min KCl arrest was equal in the two groups. No difference in mechanical energy consumption or substrate metabolism was observed between groups.
  
  
  CONCLUSIONS
  Basal MVO2 in the septic myocardium is not elevated, but an increased MVO2 for EC coupling is responsible for the energetic inefficiency.
authors.affiliation: Department of Digestive Surgery, University Hospital North Norway, Sykehusveien 38, N-9038 Tromsø, Norway.
authors.forename: Ebrahim
authors.initials: E
authors.lastname: Aghajani
authors.forename: Dag
authors.initials: D
authors.lastname: Nordhaug
authors.forename: Christian
authors.initials: C
authors.lastname: Korvald
authors.forename: Tor
authors.initials: T
authors.lastname: Steensrud
authors.forename: Kjell
authors.initials: K
authors.lastname: Husnes
authors.forename: Ole
authors.initials: O
authors.lastname: Ingebretsen
authors.forename: Arthur
authors.initials: A
authors.lastname: Revhaug
authors.forename: Truls
authors.initials: T
authors.lastname: Myrmel
mesh_terms: D000818:Animals; D002315:Cardiopulmonary Bypass; D004594:Electrophysiology; D006323:Heart Arrest; D008070:Lipopolysaccharides / Q000494:pharmacology; D008297:Male; D023421:Models, Animal; D009200:Myocardial Contraction; D010101:Oxygen Consumption; D012772:Shock, Septic / Q000150:complications / Q000378:metabolism* / Q000503:physiopathology; D013552:Swine; D018487:Ventricular Dysfunction, Left / Q000209:etiology / Q000378:metabolism* / Q000503:physiopathology
chemical_list: D008070:Lipopolysaccharides; C440499:lipopolysaccharide, Escherichia coli O111 B4