Mechanism of elevated left ventricular end-diastolic pressure after ischemic arrest and reperfusion.

The effects of ischemic arrest and reperfusion on isovolumic end-diastolic pressure, diastolic pressure-volume curves, and indices of ventricular relaxation and contractility were studied in an isolated feline heart preparation. In hearts subjected to 60 min of normothermic (37 degrees C) ischemic arrest, isovolumic developed pressure, and dP/dtmax during reperfusion returned to only approximately 60% of prearrest control levels. Isovolumic end-diastolic pressure (Ped) increased 37.0 +/- 4.3 mmHg and the time constant of ventricular relaxation was prolonged. Hearts maintained at 27 degrees C hypothermia during the 60-min ischemic period demonstrated improved contractile performance (approximately 100% of control), less elevation of Ped (21.4 +/- 4.5 mmHg), and no significant increase in the time constant of relaxation. In both groups of hearts, postarrest end-diastolic pressure-volume curves were shifted up and to the left, whereas indices of ventricular stiffness and muscle stiffness remained unchanged. These data suggest that the rise in isovolumic end-diastolic pressure observed after 1 h of ischemic arrest and reperfusion is the result of an upward and to the left shift of the entire diastolic pressure-volume relationship of the left ventricle. This shift does not appear to be related to diminished contractile performance or incomplete relaxation. Furthermore, the shift is not due to a change in muscle compliance, but to a reduction in the unstressed volume of the ventricle, which most likely results from myocardial contracture and edema.