Modeling pressure-flow relations in cardiac muscle in diastole and systole

Pressure-flow relations were calculated for a symmetrical, maximally dilated, crystalloid-perfused coronary vascular network embedded in cardiac muscle in (static) diastole and (static) systole at two muscle lengths: slack length and 90% of maximal muscle length (L(max)). The calculations are based on the ''time-varying elastance concept.'' That is, the calculations include the mechanical properties of the vascular wall and the (varying) mechanical properties of the myocardial tissue (in cross-fiber direction). We found that, at any given perfusion pressure, coronary flow is smaller in systole than in diastole. Relative reduction in vascular cross-sectional area, which forms the basis of flow impediment, was largest for the smallest arterioles. At a constant perfusion pressure of 62.5 mmHg, the transition from (static) diastole to (static) systole at constant muscle length (''isometric contraction'') was calculated to reduce flow by 74% (from 18.9 to 5.0 ml . min(-1). g(-1)) and by 64% (from 12.6 to 4.6 ml . min(-1). g(-1)) for the muscle fixed at slack length and 90% of L(max), respectively. At this perfusion pressure, contraction with 14% shortening (from 90% of L(max) in diastole to slack length in systole) was calculated to reduce flow by 61% (from 12.6 to 5.0 ml . min(-1). g(-1)). Increasing muscle length from slack length to 90% of L(max) decreases coronary flow by 34% in diastole and by 8% in systole. We conclude that modeling cardiac contraction on the basis of the time-varying elastic properties of the myocardial tissue can explain coronary flow impediment and that contractions, with or without shortening, have a larger effect on coronary flow than changes in muscle length.