Influence of caffeine and other inotropic interventions on the onset of unloaded shortening velocity in mammalian heart muscle. Time course of activation.

Abstract

The onset of maximum unloaded shortening velocity was measured in cat papillary muscles by analyzing velocity with respect to time and length after zero load clamps imposed at different times. Unloaded shortening velocity rose rapidly to a constant level by 20% of the time to peak force under all conditions studied except with application of 10 m M caffeine, which markedly slowed its onset. Load-clamping experiments showed that the force-velocity-length interrelationship which characterizes shortening remained constant throughout most of shortening except with caffeine, which delayed the onset of steady state. It is suggested that the time course of the force-velocity-length interrelationship usefully describes velocity active state , the onset of which can be measured independently of force generation at zero load. In afterloaded contractions, manifestation of velocity active state may be delayed by the slower time course of force generation which precedes shortening. It is concluded that velocity active state normally rises rapidly to a constant level which describes the contractile state. Caffeine slows the onset of velocity active state, and valid time-independent force-peak velocity curves cannot be obtained in the presence of this drug.