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June 1, 1991Acta Physiologica Scandinavica9 citations

The action of 2,3‐butanedionemonoxime on the inotropic state in guinea‐pig myocardium

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SMStellan MörnerBWBjörn Wohlfart

Structured PICO

P
Population
Isolated papillary muscles from guinea-pig right ventricles (n=9)
I
Intervention
2,3-butanedionemonoxime (BDM) 2 mM
C
Comparator
Control (baseline before drug addition)
O
Outcome
Peak twitch forcesurrogate

In isolated guinea-pig myocardium, 2,3-butanedionemonoxime significantly reduces peak twitch force and time to peak tension without altering action potential parameters or the fraction of recirculating intracellular calcium.

Abstract

Isolated papillary muscles from guinea-pig right ventricles were used (temperature 33 degrees C, stimulation frequency 0.5 Hz). Isometric twitch and action potentials were recorded. Upon addition of 2,3-butane-dionemonoxime (BDM) (2 mM) the peak twitch force was reduced from 4.17 +/- 0.4 mN/mm2 to 1.68 +/- 0.3 mN/mm2 (n = 9, P less than 0.001). The time course of the isometric twitch was slightly altered. Time to peak tension (TPT) was reduced by 12.0 +/- 3% (n = 9, P less than 0.001) whereas time to half relaxation (THR) was left unaffected. The rate of rise of force was reduced by 35 +/- 3.2 mN/mm2s i.e. 46 +/- 3%. The action potential duration and amplitude was not significantly changed by the drug. The shape of the curve relating peak twitch force of an extra beat to the preceding test interval, i.e. mechanical restitution, was affected by 2 mM 2,3-butane-dionemonoxime. The curve reached its maximum faster after addition of the drug. Maximum postextrasystolic potentiation (force in response to the prepreceding test interval) was 3.2 +/- 0.4 mN/mm2 in 2 mM 2,3-butane-dionemonoxine and 7.6 +/- 0.7 mN/mm2 in control (n = 6). However the percentage potentiation was very similar in control (82%) and in presence of 2,3-butane-dionemonoxime (91%). Peak twitch force in relation to peak force of the preceding potentiated contraction during decay of postextrasystolic potentiation was analysed. There was a linear relation between the variables, the slope being 0.34 +/- 0.04 in control and 0.30 +/- 0.02 in 2,3-butane-dionemonoxime. This suggests that the drug is without an action on the fraction of calcium recirculating within the cell.(ABSTRACT TRUNCATED AT 250 WORDS)

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Cite This Study

Mörner et al. (1991) studied this question.

synapsesocial.com/papers/6a1ebc8f6b4935698da443a9https://doi.org/10.1111/j.1748-1716.1991.tb09149.x
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Also Consider

Synapse has enriched 5 closely related papers on similar clinical questions. Consider them for comparative context:

  1. 1The electrophysiological and mechanical effects of 2,3‐butane‐dione monoxime and cytochalasin‐D in the Langendorff perfused rabbit heart2004 · 76 citations
  2. 2Mechanism of force inhibition by 2,3‐butanedione monoxime in rat cardiac muscle: roles of [Ca2+]i and cross‐bridge kinetics.1994 · 101 citations
  3. 3Contractile deactivation and uncoupling of crossbridges. Effects of 2,3-butanedione monoxime on mammalian myocardium.1991 · 168 citations
  4. 4Differential Effects of Cytochalasin D and 2, 3 Butanedione Monoxime on Isometric Twitch Force and Transmembrane Action Potential in Isolated Ventricular Muscle: Implications for Optical Measurements of Cardiac Repolarization1998 · 92 citations
  5. 5The effects of 2,3‐butanedione monoxime (BDM) on the force‐velocity relation in single muscle fibres of the frog1995 · 10 citations