Burt J M, Copeland J G
J Thorac Cardiovasc Surg. 1986 Aug;92(2):238-46.
The orthotopically transplanted heart undergoes several steps between harvest from the donor and reperfusion in the recipient: cardioplegic arrest and cooling, ischemia during the operation, in most cases a preservation or storage period of varying duration, and 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 degrees or 25 degrees 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 degrees 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 degrees 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 degrees 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 degrees 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.
心脏停搏与降温、手术期间的缺血、在大多数情况下有不同时长的保存或储存期以及再灌注。这些步骤中的每一步都代表着心脏可能遭受损伤的时期。在本研究中，我们对供体心脏在这些步骤中的每一步所遭受的损伤程度进行了量化。这一目标是通过在以下情况后经Langendorff方法评估兔心脏功能来实现的：（第1组）降温与再灌注；（第2组）心脏停搏、降温与再灌注；（第3组）停搏、降温、1小时缺血（5摄氏度或25摄氏度）与再灌注；（第4组）停搏、降温、24小时保存与再灌注；以及（第5组）停搏、降温、24小时保存、1小时缺血（25摄氏度）与再灌注。对各实验组与对照心脏进行了比较。心脏降温与再灌注（第1组）未导致功能丧失，尽管恢复到降温前功能水平大约需要25分钟。在降温前进行停搏的心脏（第2组）恢复了全部功能，且没有恢复时间延长的情况。停搏、降温并在5摄氏度下缺血的心脏（第3组）恢复了缺血前收缩功能的95%：最大收缩压和收缩压曲线的最大正导数。未检测到舒张顺应性的变化。停搏、降温并在25摄氏度下缺血的心脏（第3组）恢复了缺血前收缩功能的89%（最大收缩压和收缩压曲线的最大正导数）。同样，未检测到舒张顺应性的变化。停搏、降温、保存24小时并再灌注的心脏（第4组）恢复了对照收缩功能的84%（最大收缩压和收缩压曲线的最大正导数），而在25摄氏度下额外增加1小时缺血的心脏（第5组）仅恢复了对照收缩功能的75%。在后两组中，舒张顺应性也受到了损害。第4组达到10毫米汞柱所需的容积减少了20%，第5组减少了26%。压力 - 容积曲线表明这些心脏的收缩性和顺应性有所丧失。这些数据表明，虽然缺血和再灌注导致了显著损伤，但这种损伤被保存期导致的更大功能下降所掩盖。
