Different inotropic interventions caused distinct changes in twitch time course but similarly increased maximum velocity (1-9%) and power (5-21%) in isolated rabbit myocardium.
Do different inotropic interventions differentially affect force, velocity, and power in isolated rabbit myocardium?
Different inotropic interventions produce similar instantaneous force-velocity curves in rabbit myocardium despite varying effects on twitch time course, suggesting changes are due to activation levels rather than direct changes in contractile machinery.
To gain some insight into inotropic mechanisms, we compared the effects of several classes of inotropic interventions on the isometric twitch and force-velocity properties of isolated rabbit myocardium. Postextrasystolic potentiation was chosen as one of the interventions in the belief that its onset is so rapid that it would be unlikely to cause substantial chemical changes in the contractile proteins and that most of the effects would be due to changes in the level of activation. The effects of a digitalis analogue (acetylstrophanthidin), an adrenergic agent (isoproterenol), and a methylxanthine (caffeine) were then compared with those of postextrasystolic potentiation. The conditions were chosen so that each agent caused a twofold increase in twitch force. Acetylstrophanthidin and postextrasystolic potentiation caused twitch force to increase with only a slight (11%) decrease in time to peak force. Isoproterenol caused the peak of the twitch to occur substantially (40%) earlier with marked abbreviation of the twitch. Caffeine had the opposite effect: time to peak force was delayed (by 60%), and the twitch was markedly prolonged. In contrast to the marked differences in the time course of the twitch, there was no significant difference between the instantaneous force-velocity curves obtained with the different interventions. All four interventions caused maximum velocity to increase slightly (1-9%) and maximum power to increase only slightly more than twitch force (5-21%). All of the changes observed can be accounted for by changes in activation, either by an increase in the amount of calcium released into the myofilament space or by a change in the sensitivity of the myofilaments to calcium. There was no need to postulate direct changes in the contractile machinery to account for these results.
Chiu et al. (Wed,) conducted a other in Isolated rabbit myocardium. Inotropic interventions (postextrasystolic potentiation, acetylstrophanthidin, isoproterenol, caffeine) vs. Comparison among different interventions was evaluated on Isometric twitch and force-velocity properties. Different inotropic interventions caused distinct changes in twitch time course but similarly increased maximum velocity (1-9%) and power (5-21%) in isolated rabbit myocardium.
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