Successful survival of primates receiving transplantation with "dead," nonbeating donor hearts

Abstract

A paucity of donor organs is the principal limitation in human heart transplantation. Prompted by our short-term studies of reanimating "dead" donor hearts in sheep, we applied the same reperfusion modifications in juvenile baboons to determine human applications in an anoxic arrest model (as occurs when non-brain-dead patients are extubated and allowed to die). Ten juvenile baboons (mean weight 3.6 kg) were studied. Five baboons were used as donors. After being anesthetized, donors were pretreated with methylprednisolone (Solu-Medrol), 50% dextrose, nifedipine, and prostaglandin E 1 and then paralyzed and extubated. Donors became pulseless at 7 ± 1 minutes and had electric arrest 9 to 18 minutes after paralysis. The five donors were left undisturbed and warm for 15, 22, 30, 30, and 31 minutes, respectively, after asystole. They were then given 250 ml of 4° C Roe's crystalloid cardioplegic solution via the aortic root and the hearts were explanted into iced Euro-Collins solution. Five baboons served as recipients. After donor harvest, recipients were placed on cardiopulmonary bypass, given prostaglandin E 1 , and cooled to 18° C; circulatory arrest was instituted and the recipient's heart excised. The donor heart was transplanted in an orthotopic position. Before reinstitution of bypass, 250 ml of terminal leukocyte-depleted blood cardioplegic solution was given, then bypass was restarted and the hearts were reperfused for 60 minutes. All animals were weaned from bypass without the use of inotropic agents. All animals were extubated within 2 to 4 hours after bypass and received standard immunosuppression. Peak creatine kinase MB/total creatine kinase ratio was 0.2% ± 0.2%. Postoperative ejection fractions by echocardiography were 75% to 80% (mean 76%). Animals survived 1, 9, 13, 16, and 34 days, with three deaths caused by acute rejection and one each by stroke and diarrhea/dehydration. Pathologic findings showed no areas of fibrosis or ischemic damage. We conclude that successful reanimation and engraftment can be achieved with the use of the asystolic primate heart; this work suggests that human application is realistic and could greatly expand the donor pool. (J T HORAC C ARDIOVASC S URG 1995;109:1097-102)