title: Adaptation of the right ventricle to an increased afterload in the chronically volume overloaded heart.
abstract: BACKGROUND
  Increased right ventricular afterload is a common problem after correction of various heart diseases with chronic volume overload. We determined the effects of an acute increase of right ventricular afterload in normal and chronically volume overloaded hearts.
  
  
  METHODS
  In 6 dogs, volume overload was induced by chronic arteriovenous shunts for 3 months. Six sham-operated animals served as controls. After closing the shunts, right ventricular systolic and end-diastolic pressure as well as end-diastolic volume were measured by conductance catheter. In addition, pressure-volume loops were recorded. Myocardial contractility was described by the slope of the end-systolic pressure-volume relationship. Afterload was increased to right ventricular systolic pressure to 35 mm Hg and to 50 mm Hg by pulmonary banding.
  
  
  RESULTS
  Chronic volume overload resulted in a significant increase of right ventricular systolic pressure (34 +/- 2 versus 25 +/- 2 mm Hg, p < 0.05), end-diastolic pressure (10.4 +/- 1.7 versus 6.8 +/- 0.4 mm Hg, p < 0.05), and end-diastolic volume (39 +/- 2 versus 33 +/- 3 mL, p < 0.05). Baseline contractility (1.47 +/- 0.24 versus 1.53 +/- 0.32 mm Hg/mL) did not differ. While afterload increase to 35 and 50 mm Hg led to stepwise increase in contractility (2.73 +/- 0.30 mm Hg/mL and 4.15 +/- 0.30 mm Hg/mL, p < 0.05 versus baseline, respectively) at unchanged end-diastolic pressure and volume in controls, it showed only a slight increase (2.11 +/- 0.38 mm Hg/mL and 2.99 +/- 0.29 mm Hg/mL, p < 0.05 versus sham) with concomitant increase in end-diastolic pressure (12.4 +/- 2.2 mm Hg/mL and 16.3 +/- 1.9 mm Hg, p < 0.05) and volume (42 +/- 4 mL and 48 +/- 8 mL, p < 0.05) in the chronically volume overloaded group.
  
  
  CONCLUSIONS
  Chronic volume overload per se does not impair right ventricular contractility. However, the inotropic adaptation (homeometric autoregulation) to an increased afterload is limited, which is partly compensated by the Frank-Starling mechanism (heterometric autoregulation).
authors.affiliation: Department of Cardiac Surgery, University of Heidelberg, Heidelberg, Germany. dzsi@hotmail.com
authors.forename: Gábor
authors.initials: G
authors.lastname: Szabó
authors.forename: Pál
authors.initials: P
authors.lastname: Soós
authors.forename: Susanne
authors.initials: S
authors.lastname: Bährle
authors.forename: Tamás
authors.initials: T
authors.lastname: Radovits
authors.forename: Ernst
authors.initials: E
authors.lastname: Weigang
authors.forename: Violetta
authors.initials: V
authors.lastname: Kékesi
authors.forename: Béla
authors.initials: B
authors.lastname: Merkely
authors.forename: Siegfried
authors.initials: S
authors.lastname: Hagl
mesh_terms: D000222:Adaptation, Physiological; D000818:Animals; D001166:Arteriovenous Shunt, Surgical / Q000009:adverse effects; D002302:Cardiac Output; D002908:Chronic Disease; D004195:Disease Models, Animal; D004285:Dogs; D005263:Femoral Artery / Q000601:surgery; D005268:Femoral Vein / Q000601:surgery; D006352:Heart Ventricles / Q000503:physiopathology*; D006439:Hemodynamics; D009200:Myocardial Contraction; D011312:Pressure / Q000009:adverse effects; D013318:Stroke Volume