ArticlePflugers Archiv : European journal of physiology1996
Effects of 2,3-butanedione monoxime on cross-bridge kinetics in rat cardiac muscle.
Article in Pflugers Archiv : European journal of physiology, 1996. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 21 citations in OpenAlex.
- Generation of myocyte agonal CaScientific reports · 2023Article
- The Frank-Starling mechanism involves deceleration of cross-bridge kinetics and is preserved in failing human right ventricular myocardium.American journal of physiology. Heart and circulatory physiology · 2015Article
- Troponin I phosphorylation enhances crossbridge kinetics during beta-adrenergic stimulation in rat cardiac tissue.The Journal of physiology · 2002Article
- Effects of 2,3-butanedione monoxime (BDM) on calcium channels expressed in Xenopus oocytes.The Journal of physiology · 1998Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The effects of 2,3-butanedione monoxime (BDM) on isometric force and myofibrillar adenosine 5'-triphosphatase (ATPase) activity were studied in skinned cardiac trabeculae from the rat. ATP hydrolysis was enzymatically coupled to the breakdown of reduced nicotinamide adeninedinucleotide (NADH). The NADH concentration was monitored photometrically. Measurements were performed at a sarcomere length of 2.1 microm, 20 degrees C and pH 7.0. Without BDM, isometric force was 45 +/- 3 kN/m2 and the isometric ATPase activity 0.49 +/- 0.04 mM/s (mean +/- SEM, n = 31). Force gradually decreased as a function of [BDM] to 2.8 +/- 0.4% at 100 mM BDM. ATPase activity was also depressed by BDM, but to a lesser extent than force. BDM therefore has a marked effect on myofibrillar tension cost. The rate of tension redevelopment after unloaded shortening decreased from 29 +/- 2 s-1 (n = 10) without BDM to 22 +/- 1 s-1 (n = 5) at 20 mM BDM. These results, modelled in a two- and three-state scheme of cross-bridge interaction, indicate that, in cardiac muscle, BDM not only affects cross-bridge formation but, especially at high concentrations (>/= 20 mM), also causes a marked increase in the apparent rate of cross-bridge detachment.
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