title: Acute and chronic changes of myocardial energetics in the mammalian and human heart.
abstract: In earlier studies using papillary muscles of the rat left ventricle and highly sensitive thermopiles we demonstrated that the heat liberated per gram of myocardium per unit of developed tension-time integral is decreased when the rats suffered from hypothyroidism or renal hypertension. This increase in economy of force production was shown to be associated with a decrease in myosin-ATPase activity and a change in isomyosin composition. In a recent study we showed an increase in heat per gram of mammalian myocardium per tension-time integral of 70% after application of isoproterenol. In order to study the relationship between energy costs and developed tension-time integral in the human heart, haemodynamics and myocardial oxygen consumption were measured. The data were obtained using a Millar microtip catheter pressure transducer and the argon method. Haemodynamics and myocardial energetics were analysed in 8 patients without significant heart disease before and after application of isoproterenol and in 10 patients with dilative cardiomyopathy (NYHA II-III). During one cardiac cycle, myocardial oxygen consumption per gram of LV myocardium per beat (MVO2/g x beat) is related to LV stress-time integral (integral of sigma xt). The economy of myocardial contraction (EC) was calculated by (formula; see text) EC was 11.3 +/- 3.2 in normal and 14.3 +/- 4.7 dyn x s x g/cm2 x mu cal in dilative cardiomyopathic hearts (NS). Isoproterenol decreased EC from 11.3 +/- 3.2 to 5.5 +/- 1.6 dyn x s x g/cm2 x mu cal in the normal hearts (p less than 0.01). In the rat myocardium, changes in economy of force generation were found due to catecholamines, pressure overload and hypothyroidism. In the human heart, similar energetic changes were observed due to catecholamines. No significant differences in energy of force production were seen between normal and dilative cardiomyopathic hearts. The effect of catecholamines in the mammalian and human myocardium is explained by changes in activation processes and in chemomechanical energy transduction at the level of the contractile proteins.
authors: Medizinische Klinik III, Universität Freiburg, F.R.G.
authors: C
authors: C
authors: Holubarsch
authors: G
authors: G
authors: Hasenfuss
authors: H W
authors: HW
authors: Heiss
authors: T
authors: T
authors: Meinertz
authors: H
authors: H
authors: Just
mesh_terms: D000208:Acute Disease; D000818:Animals; D009202:Cardiomyopathies / Q000378:metabolism / Q000503:physiopathology; D002908:Chronic Disease; D004734:Energy Metabolism; D006321:Heart / Q000503:physiopathology; D006331:Heart Diseases / Q000378:metabolism / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction; D009206:Myocardium / Q000378:metabolism