title: The contraction of stunned myocardium: isovolumetric bulging and wasted ejection shortening in dog heart.
abstract: OBJECTIVE
  The aim of the study was to assess the contraction of myocardium stunned by repetitive brief coronary occlusions by examining the response to alterations in loading and inotropy of systolic contraction on isovolumetric and ejection phase shortening.
  
  
  METHODS
  Fourteen open chest anaesthetised dogs were used for the studies. After destruction of the sinus node, the heart was atrially paced and atrial extrasystoles were introduced followed by a short (400 ms) or long (700 ms) postextrasystole. The left anterior descending coronary artery was occluded for 5 min and reperfused for 10 min a total of eight times to produce stunned myocardium, followed by a final 60 min of reflow. Regional function was assessed with segment length sonomicrometers.
  
  
  RESULTS
  With successive periods of occlusion there was an increase in the end diastolic segment length and a progressive decrease in total percent systolic shortening (baseline 22.3%, 1st reflow 14.5%, 8th reflow 7.9%) with some recovery after 60 min of reflow (12.0%). This was predominantly due to the development of bulging during isovolumetric systole (4.5%, -4.9%, and -8.3%, respectively) which diminished during 60 min recovery to -3.1%. Ejection shortening was relatively constant (17.8%, 19.4%, 16.3%, and 15.1%, respectively). Postextrasystolic potentiation resulted in an increased in total percent systolic shortening, but not to the baseline value, as slight isovolumetric bulging persisted. Similar changes were seen with the short and long postextrasystoles although the latter had a greater increase in ejection shortening.
  
  
  CONCLUSIONS
  The decrease in function after repetitive occlusion and reflow is predominantly due to bulging during isovolumetric systole which persists after postextrasystolic potentiation in our model of stunned myocardium.
authors.affiliation: Philadelphia Heart Institute, Presbyterian Medical Center, Pennsylvania.
authors.forename: G
authors.initials: G
authors.lastname: Chen
authors.forename: A D
authors.initials: AD
authors.lastname: Askenase
authors.forename: K
authors.initials: K
authors.lastname: Chen
authors.forename: L N
authors.initials: LN
authors.lastname: Horowitz
authors.forename: B L
authors.initials: BL
authors.lastname: Segal
mesh_terms: D000818:Animals; D002304:Cardiac Pacing, Artificial; D003327:Coronary Disease / Q000503:physiopathology; D004195:Disease Models, Animal; D004285:Dogs; D009200:Myocardial Contraction / Q000502:physiology*; D015428:Myocardial Reperfusion Injury / Q000503:physiopathology*; D013318:Stroke Volume / Q000502:physiology; D013599:Systole