Adaptation of left ventricle to chronic pressure overload: response to inotropic drugs.
Left ventricular (LV) force-generating capacity was determined in eight anesthetized dogs with pressure-overload hypertrophy. Length-contractile force (CF) curves recorded from the LV with a modified Walton-Brodie arch were displaced upward from control. However, when CF was normalized for LV wall thickness changes accompanying hypertrophy and expressed as g/cm2, the length-CF curve was depressed compared to normal. The CF response to isoproterenol and calcium was depressed in dogs with hypertrophy; however, the CF response to ouabain was not different from control. Taken collectively these findings suggest that pressure-overload hypertrophy is associated with a depressed force-generating capacity per unit cross section of myocardium at any given muscle length, i.e., a depressed inotropic state, but that the hypertrophied LV has a greater than normal force-generating capacity due to an increased number of weaker cross-sectional units. Further, the depressed inotropic state is not associated with augmented plasma norepinephrine levels. Therefore, adaptation of the LV to pressure overload is by cardiac hypertrophy alone.
D000818:Animals; D002118:Calcium / Q000494:pharmacology; D002306:Cardiac Volume; D006332:Cardiomegaly / Q000097:blood / Q000503:physiopathology; D004285:Dogs; D004305:Dose-Response Relationship, Drug; D006321:Heart / Q000502:physiology*; D007545:Isoproterenol / Q000494:pharmacology; D009200:Myocardial Contraction / Q000187:drug effects*; D009638:Norepinephrine / Q000097:blood; D010042:Ouabain / Q000494:pharmacology
D010042:Ouabain; D007545:Isoproterenol; D002118:Calcium; D009638:Norepinephrine