[Unloaded shortening velocity of the myocardium as an index of contractility (author's transl)].
An experimental study attempts to clarify the reasons for a fashionable over- or underestimation of the unloaded shortening velocity of the myocardium (Vmax) as an index of "contractility" in international cardiological literature. Long-term investigations on the isolated myocardial preparation as well as on the heart in situ support our own position: 1. Vmax of the myocardium is, without doubt, a value of greater relevance in muscle physiology independent of the interpretation related to the fundamental processes. 2. Vmax cannot be exclusively regarded as a function of the rate of cross-bridge movements, but is influenced by the Ca2+-concentration and consequently by the conditions of electromechanical coupling. 3. Vmax is not a reliable measure for myocardial power capacity under all conditions as this value on the one hand and the developed tension on the other are influenced to different degrees. 4. If the amount of contractile material per cross sectional unit is changed (changed relation of fibrils/mitochondria), Vmax can give better indications on the contractile elementary process than the developed tension. 5. Increased content of connective tissue and scars influence both the developed tension and Vmax. 6. A reduction in Vmax under long-term increased hemodynamic loading of the heart is not to be considered a priori as an expression of cellular damage.
D000818:Animals; D002118:Calcium / Q000502:physiology; D006332:Cardiomegaly; D002415:Cats; D006321:Heart / Q000502:physiology*; D009200:Myocardial Contraction; D009206:Myocardium / Q000648:ultrastructure; D051381:Rats
D002118:Calcium
Die lastfreie Verkürzungsgeschwindigkeit des Myokards als Kontraktilitätsmass.