Hyperfunction with normal inotropic state of the hypertrophied left ventricle.
Conscious dogs were instrumented with an inflatable cuff around the ascending aorta, a high-fidelity micromanometer in the left ventricle (LV), and pairs of ultrasonic crystals for measurements of LV wall thickness and internal LV diameter. Wall stress (WSt) and mean velocity of wall shortening (VCF) were calculated. Mean force-velocity relations and WSt-diameter loops in single contractions were then analyzed over a range of matched systolic pressures during acute aortic constrictions both before and after induction of chronic hypertrophy by sustained aortic constriction. At normal LV systolic pressures and at each matched level of systolic LV pressure, wall shortening velocity was increased in the hypertrophied ventricle. However, force-velocity relations obtained by relating mean VCF to mean WSt at various stress levels fell on the same relation as during control. The linear relation between LV diameter and pressure at the end of ventricular ejection was shifted to the left in the hypertrophied ventricle, indicating enhanced shortening. However, linear WSt-diameter relations at end-ejection were not different in control and hypertrophied hearts. These findings indicate that the ventricle hypertrophied by pressure overload exhibited hyperfunction as a pump but that its myocardium had a normal level of inotropic state.
D000818:Animals; D001024:Aortic Valve Stenosis / Q000150:complications; D001794:Blood Pressure; D006332:Cardiomegaly / Q000209:etiology / Q000503:physiopathology*; D004285:Dogs; D006321:Heart / Q000503:physiopathology*; D009200:Myocardial Contraction; D013314:Stress, Mechanical