Literature DB >> 2373999

Spontaneous contractions in rat cardiac trabeculae. Trigger mechanism and propagation velocity.

M C Daniels1, H E ter Keurs.   

Abstract

It has previously been observed that spontaneous contractions start in a region of damage of isolated right ventricular trabeculae of rat, propagate along the muscle, and induce triggered arrhythmias (Mulder, B.J.M., P.P. de Tombe, and H.E.D.J. ter Keurs. 1989. J. Gen. Physiol. 93:943-961). The present study was designed to analyze the mechanisms that lead to triggered propagated contractions (TPCs). TPCs were elicited in 29 trabeculae by stimulation with trains (2 Hz; 15-s intervals) at varied number of stimuli (n), lowered temperature (19-21 degrees C), and varied [Ca++]o (1.5-4 mM) in the superfusate. Length (SL) and shortening of sarcomeres in the muscle were measured at two sites using laser diffraction techniques; twitch force (Ft) was measured with a silicon strain gauge. Time between the last stimulus in the train and the onset of sarcomere shortening due to a TPC at a site close to the damaged end region (latency) and propagation velocity of the contraction (Vprop) were correlated with Ft. For 10 trabeculae, TPCs were calculated to start in the end region itself 586 +/- 28 ms (mean +/- 1 SEM) after the last stimulus of a train (n = 15; [Ca++]o: 1.5 mM), i.e., at the end of or after the rapid release of the damaged end during twitch relaxation. When Ft was increased by increasing either SL prior to stimulation or the afterload during twitches, methods that do not affect intracellular calcium levels, latency decreased, but Vprop remained constant. No TPC occurred when Ft was less than 20% of maximal Ft. Both increasing [Ca++]o and n increased Ft to a maximum, increased Vprop progressively (maximum Vprop, 17 mm/s), but decreased latency. These observations suggest that initiation of TPCs depends on the force developed by the preceding twitch, and therefore on the degree of stretch and subsequent rapid release of damaged areas in the myocardium, while Vprop along the trabeculae is determined by intracellular calcium concentration.

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Year:  1990        PMID: 2373999      PMCID: PMC2216350          DOI: 10.1085/jgp.95.6.1123

Source DB:  PubMed          Journal:  J Gen Physiol        ISSN: 0022-1295            Impact factor:   4.086


  31 in total

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Authors:  H G Glitsch; L Pott
Journal:  Pflugers Arch       Date:  1975-07-09       Impact factor: 3.657

2.  Myocardial sarcomere dynamics during isometric contraction.

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Journal:  J Physiol       Date:  1975-10       Impact factor: 5.182

3.  Excitation-contraction coupling of isolated cardiac fibers with disrupted or closed sarcolemmas. Calcium-dependent cyclic and tonic contractions.

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4.  Sarcomere motion in isolated cardiac cells.

Authors:  G Rieser; R Sabbadini; P Paolini; M Fry; G Inesi
Journal:  Am J Physiol       Date:  1979-01

5.  Protective action of calcium channel antagonist agents against ventricular fibrillation in the isolated perfused rat heart.

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8.  Diastolic scattered light fluctuation, resting force and twitch force in mammalian cardiac muscle.

Authors:  E G Lakatta; D L Lappé
Journal:  J Physiol       Date:  1981-06       Impact factor: 5.182

9.  Tension development and sarcomere length in rat cardiac trabeculae. Evidence of length-dependent activation.

Authors:  H E ter Keurs; W H Rijnsburger; R van Heuningen; M J Nagelsmit
Journal:  Circ Res       Date:  1980-05       Impact factor: 17.367

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Authors:  M Chiesi; M M Ho; G Inesi; A V Somlyo; A P Somlyo
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  8 in total

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8.  Magnetic Resonance Imaging of Contracting Ultrathin Cardiac Tissue.

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  8 in total

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