作者: James T. Pearson , Mikiyasu Shirai , Hirotsugu Tsuchimochi , Daryl O. Schwenke , Takayuki Ishida
DOI: 10.1529/BIOPHYSJ.107.111740
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摘要: The cellular basis of the length-dependent increases in contractile force beating heart has remained unclear. Our aim was to investigate whether mediated are correlated with myosin head proximity actin filaments, and presumably number cross-bridges activated during a contraction. We therefore employed x-ray diffraction analyses beat-to-beat contractions spontaneously rat hearts under open-chest conditions simultaneous recordings left ventricle (LV) pressure-volume. Regional patterns were recorded from anterior LV free wall steady-state acute volume loading (intravenous lactate Ringers infusion at 60 ml/h, <5 min duration) determine change intensity ratio (I(1,0)/I(1,1)) interfilament spacing (d(1,0)). found no significant end-diastolic (ED) ratio, indicating that proportion heads unchanged by fiber stretching. Intensity decreased significantly more isovolumetric contraction phase than baseline contractions. A systolic increase filaments maximum rate pressure increase. Hence, reduction end-diastole ( approximately 0.5 nm) stretch increased activated. Furthermore, our suggest d(1,0) expansion inversely related but restricted sarcomere shortening values smaller relaxation. Since ventricular volume, length, be directly spacing, these findings support role for modulating cross-bridge formation developed before shortening.