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.