title: Change in aortic end-systolic pressure by alterations in loading sequence and its relation to left ventricular isovolumic relaxation.
abstract: BACKGROUND
  A brief, sustained constriction of the descending and the ascending aortas produces systolic loads at different times during ejection, and descending intervention prolongs left ventricular (LV) relaxation more than ascending intervention. Although alterations in the sequence of loading the ventricle have been suggested as a cause of such load-induced relaxation abnormalities, the relation of the loading system to relaxation has been unclear.
  
  
  RESULTS
  LV peak systolic pressure was elevated by approximately 40 mm Hg by constricting the descending and ascending aortas in seven anesthetized dogs. The descending intervention increased aortic end-systolic pressure (AoESP, 110.4 +/- 9.3 to 150.8 +/- 11.5 mm Hg; P < .05), reduced aortic flow (P < .05), and prolonged LV relaxation (time constant [T], 31.9 +/- 4.4 to 69.8 +/- 12.8 ms; P < .05). LV ejection time was reduced, but the systolic time interval was unchanged. In contrast, ascending intervention decreased AoESP (111.9 +/- 11.4 to 101.5 +/- 10.3 mm Hg; P < .05), reduced aortic flow (P < .05), and prolonged T (31.2 +/- 5.4 to 42.2 +/- 8.3 ms; P < .05), whereas ejection time and systolic time interval increased (both P < .01). Prolongation of T was significantly greater during descending intervention (P < .05) and was associated with an increase in AoESP during descending intervention but a decrease in AoESP during ascending intervention.
  
  
  CONCLUSIONS
  Descending intervention induced greater prolongation of T than ascending intervention. Prolongation of T was closely related to an increase in AoESP in the descending intervention but a decrease in AoESP in the ascending intervention. These data suggest that not only the loading sequence but also the pressure level at the onset of isovolumic relaxation determines LV relaxation.
authors.affiliation: Department of Internal Medicine, Faculty of Medicine, Kyoto University, Japan.
authors.forename: F
authors.initials: F
authors.lastname: Kohno
authors.forename: T
authors.initials: T
authors.lastname: Kumada
authors.forename: M
authors.initials: M
authors.lastname: Kambayashi
authors.forename: W
authors.initials: W
authors.lastname: Hayashida
authors.forename: N
authors.initials: N
authors.lastname: Ishikawa
authors.forename: S
authors.initials: S
authors.lastname: Sasayama
mesh_terms: D000818:Animals; D001011:Aorta / Q000502:physiology*; D001013:Aorta, Thoracic; D001794:Blood Pressure / Q000502:physiology*; D002118:Calcium / Q000502:physiology; D003250:Constriction; D004285:Dogs; D006339:Heart Rate; D008954:Models, Biological; D009126:Muscle Relaxation; D009200:Myocardial Contraction; D013318:Stroke Volume; D013599:Systole / Q000502:physiology*; D014655:Vascular Resistance; D016277:Ventricular Function, Left / Q000502:physiology*
chemical_list: D002118:Calcium