Myocardial function after preservation for 24 hours

The orthotopically transplanted heart undergoes several steps between harvest from the donor and reperfusion in the recipient: (1) cardioplegic arrest and cooling, (2) ischemia during the operation, (3) in most cases a preservation or storage period of varying duration, and (4) reperfusion. Each of these steps represents a period during which damage to the heart can occur. In this study we have quantified the degree of damage sustained by a donor heart during each of these steps. This objective was achieved by evaluating the function of rabbit hearts via Langendorff procedures following (Group 1) cooling and reperfusion; (Group 2) cardioplegic arrest, cooling, and reperfusion; (Group 3) arrest, cooling, 1 hour of ischemia (5° or 25° C), and reperfusion; (Group 4) arrest, cooling, 24 hours of preservation, and reperfusion; and (Group 5) arrest, cooling, 24 hours of preservation, 1 hour of ischemia (25° C), and reperfusion. Comparisons were made between groups and to control hearts. Cooling and reperfusing the heart (Group 1) led to no loss of function, although recovery to precooling function levels required approximately 25 minutes. Hearts that were arrested before cooling (Group 2) regained full function without the slow recovery time. Hearts that were arrested, cooled, and made ischemic at 5° C (Group 3) recovered 95% of preischemic contractile function: maximum systolic pressure and the maximum positive derivative of the systolic pressure curve. No change in diastolic compliance was detected. Hearts that were arrested, cooled, and made ischemic at 25° C (Group 3) recovered 89% of preischemic contractile function (maximum systolic pressure and the maximum positive derivative of the systolic pressure curve). Again, no change in diastolic compliance was detected. Hearts that were arrested, cooled, preserved for 24 hours, and reperfused (Group 4) recovered 84% of control contractile function (maximum systolic pressure and the maximum positive derivative of the systolic pressure curve), whereas hearts that had the additional hour of ischemia at 25° C (Group 5) recovered only 75% of control contractile function. In the latter two groups diastolic compliance was also compromised. Group 4 had a 20% decrease in the volume required to reach 10 mm Hg, and Group 5 had a 26% decrease. Pressure-volume curves suggest a loss of contractility and a loss of compliance in these hearts. These data indicate that while significant damage occurred as a result of ischemia and reperfusion, this damage was masked by the larger decrease in function occurring as a result of the preservation period.