Angiotensin II administration at 100% Lmax decreased developed tension by 37% in infarcted rat myocardium and 12% in controls, but increased tension at shorter muscle lengths.
To determine whether changes in sarcomere length affect the inotropic response of the heart to angiotensin II (ANG II) differently in dilated and failing myocardium, papillary muscles were removed 2 days after infarction, and the effects of ANG II were studied at various muscle lengths. Myocardial infarction, which averaged 52% of the left ventricle inclusive of the interventricular septum, was characterized hemodynamically by left ventricular failure and right ventricular dysfunction. ANG II administration at 100% the muscle length where force development is maximal (Lmax) produced a 12% depression of developed tension in papillary muscles from noninfarcted ventricles and a 37% decrease in developed tension in the viable myocardium of infarcted rats. In contrast, at 85 and 92.5% Lmax and in the presence of ANG II, control muscles increased active tension by 16 and 1.0%, whereas muscles from coronary occluded hearts augmented developed tension by 13 and 22%, respectively. In conclusion, ANG II exerted a positive inotropic effect on rat myocardium at muscle lengths on the ascending limb of the Starling curve but a negative inotropic action at the muscle length normally associated with maximum force development. This phenomenon emphasizes that hormonal influences on the contractile state of the diseased heart may be modulated by the interaction of end-diastolic pressure, sarcomere length, and ventricular size and shape.
Li et al. (Tue,) conducted a other in Myocardial infarction. Angiotensin II (ANG II) vs. Noninfarcted ventricles (control) was evaluated on Developed tension in papillary muscles at various muscle lengths. Angiotensin II administration at 100% Lmax decreased developed tension by 37% in infarcted rat myocardium and 12% in controls, but increased tension at shorter muscle lengths.