A common mechanism for concurrent changes of diastolic muscle length and systolic function in intact hearts

Mechanical properties of the myocardium at end diastole have been thought t o be dominated by passive material properties rather than by active sarcome re cross- bridge interactions. This study tested the hypothesis that residu al cross- bridges significantly contribute to end-diastolic mechanics in vi vo and that changes in end- diastolic cross- bridge interaction parallel co ncurrent changes in systolic cross- bridge interaction. Open- chest anesthe tized pigs were treated with intracoronary verapamil (n = 7) or 2,3-butaned ione monoxime (BDM; n = 8). Regional left ventricular external work and end - diastolic pressure (EDP) versus end- diastolic segment length (EDL) relat ions were determined in the treated and untreated regions of each heart. Bo th agents reduced external work of treated regions to 31- 38% of baseline a nd concurrently shifted EDP versus EDL relations to the right (i. e., great er EDL at a given EDP) by an average of 5% (P < 0.05). During washout of th e drugs, EDP versus EDL returned to baseline in parallel with recovery of e xternal work. Sarcomere length, measured by transmission electron microscop y in BDM- treated and untreated regions of the same hearts after diastolic arrest and perfusion fixation, was 8% greater in BDM- treated regions (P < 0.01). We concluded that residual diastolic cross- bridges significantly an d reversibly influence end- diastolic mechanics in vivo. Alterations of end - diastolic and systolic cross- bridge interactions occur in parallel.