We demonstrate using synchrotron x-ray radiation that length-dependent mechanisms influence cross-bridge cycling in in situ rat hearts, and then describe the effects of ischaemia-reperfusion on contractility. All experiments were performed in real time using synchrotron radiation at Spring-8 and x-ray diffraction techniques. Mass transfer of myosin to actin during contraction was inferred from the change in diffraction intensity ratio (intensity of 1,0 reflection / 1,1 reflection) derived from the myosin-actin filaments in fibres. Sustained volume loading by infusion of sodium lactate (40-60 ml/h for <5 min) evoked a rightward shift in left ventricular volume and significant decreases in epicardial myosin spacing, consistent with sarcomere stretching. Increases in stroke volume were correlated with increases in mass transfer and myosin spacing change. Local comparisons of intensity ratio and myosin spacing cycles during ischaemia-reperfusion indicate that 1) mass transfer in the damaged area was reduced by moderate ischaemia, and sometimes unsynchronised, 2) compensatory increases in contractility were detected in non-ischaemic areas (and during reperfusion), and 3) myosin spacing increases were reduced and delayed or reversed under severe ischaemia. These findings suggest that non-functional fibres are stretched under high cardiac output during acute ischaemia. [J Physiol Sci. 2006;56 Suppl:S58]
