title: The effects of acute afterload change on systolic ventricular function in conscious dogs with normal vs. failing hearts.
abstract: BACKGROUND
  To date, no data exist on the linearity and, therefore, the usefulness of the preload recruitable stroke work (PRSW) and end-systolic pressure-volume (ESPVR) relationships during acute afterload changes in heart failure.
  
  
  OBJECTIVE
  Our aim was, therefore, to characterize both relationships in a model of ventricular pacing induced heart failure at baseline and during acute changes in afterload.
  
  
  METHODS
  Dynamic left ventricular volume and transmural pressure were measured in 10 conscious dogs using sonomicrometry and micromanometry under control conditions and during heart failure produced by 3 weeks of rapid right ventricular pacing. Afterload was varied from baseline with intravenous infusions of nitroprusside and phenylephrine. Left ventricular function was assessed using the PRSW and ESPVR relationships.
  
  
  RESULTS
  Cardiac output demonstrated a linear inverse relationship with afterload in both normal and failing hearts (r2>0.5, P<0.001) with failure producing a parallel, downward shift of the afterload (x) vs. cardiac output (y) relationship (P<0.01). Yet, afterload variation did not affect PRSW or ESPVR relationships in either normal or failing hearts (r2<0.12, P>0.05).
  
  
  CONCLUSIONS
  Thus, the PRSW and ESPVR relationships are insensitive to acute afterload changes in both failing and normal hearts, and the failing left ventricle is no more afterload-sensitive than the normal heart.
authors.affiliation: Departments of Thoracic Surgery, Box 3851, Duke University Medical Center, Durham, NC 27710, USA.
authors.forename: Richard B
authors.initials: RB
authors.lastname: Thompson
authors.forename: Ewout J
authors.initials: EJ
authors.lastname: van den Bos
authors.forename: David J
authors.initials: DJ
authors.lastname: Esposito
authors.forename: Clarence H
authors.initials: CH
authors.lastname: Owen
authors.forename: Donald D
authors.initials: DD
authors.lastname: Glower
mesh_terms: D000818:Animals; D001794:Blood Pressure; D002302:Cardiac Output / Q000502:physiology; D002304:Cardiac Pacing, Artificial; D004195:Disease Models, Animal; D004285:Dogs; D004452:Echocardiography; D006333:Heart Failure / Q000503:physiopathology*; D016014:Linear Models; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D013318:Stroke Volume / Q000187:drug effects / Q000502:physiology*; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D014665:Vasodilator Agents / Q000494:pharmacology; D016277:Ventricular Function, Left / Q000187:drug effects / Q000502:physiology*
chemical_list: D014662:Vasoconstrictor Agents; D014665:Vasodilator Agents; D009599:Nitroprusside; D010656:Phenylephrine