Progressive coronary vasoconstriction during 25 hours of myocardial preservation in vitro impairs functional capacity following preservation

We have developed perfusion techniques for preserving rat hearts for 25 h and have quantified haemodynamic function after preservation to establish the relation between coronary vascular resistance during preservation and the quality of postpreservation pump function. Thirteen rat hearts underwent hypothermic (8°C), low-pressure (15 mmHg) perfusion with an hyperosmotic (385 mOsm/l) crystalloid preservation buffer for 25 h. During this period, the coronary flow rate decreased from 1.12±0.28 ml/min to 0.87±0.12 ml/min (±SD). Following the preservation period, the quality of pump function was tested in the isolated working heart model. At a fixed value of left atrial pressure (15 mmHg), the afterload was increased stepwise (5 mmHg) from 45 mmHg to 70 mmHg, making use of a Starling resistor in series with an air compliance. Each afterload step was maintained for 5 min to obtain stable readings of cardiac output and coronary flow. These measurements were compared with those from a control group of 10 rat hearts undergoing the same test protocol for haemodynamic function without previous preservation. The 13 hearts which underwent 25 h preservation had subnormal haemodynamic function: cardiac output was 50%±4% compared to 10 control hearts. If preserved hearts were divided into two groups based on coronary vascular resistance measured at the end of the preservation period lower than 18 mmHg · min per ml (group 1), and higher than or equal to 18 mmHg · min per ml (group 2), it appeared that the haemodynamic function of group 2 hearts was about half that of group 1 hearts. It is concluded that the haemodynamic function of rat hearts following preservation is negatively affected by coronary vasoconstriction occurring during preservation.