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Ann Thorac Surg 2002;73:1614-1615
© 2002 The Society of Thoracic Surgeons
a Cardiac Transplant Research Group, Division of Cardiac Surgery, University of Toronto, Toronto General Hospital, EN 14-215, 200 Elizabeth St, Toronto, ON M5G 2C4, Canada
e-mail: paul.fedak{at}utoronto.ca
Improved methods of cardioplegia delivery, temperature, and composition have contributed to the excellent outcomes obtained with routine cardiac surgery. However, improved methods of cardiac protection during storage for transplantation has not proceeded with the same results. Alamanni and coworkers maintain that the endothelium plays a pivotal role in the recovery of myocardial metabolism and function following cardiac preservation, and that equal efforts should be made to protect both endothelial cells and cardiomyocytes from injury during storage [1]. Endothelial dysfunction induced during storage may have multiple adverse effects, including early graft dysfunction and late complications such as accelerated coronary vascular disease. Research efforts aimed at determining the role of the endothelium in mediating graft dysfunction, and subsequent efforts to prevent these adverse effects, may extend the safe duration of organ storage and improve the long-term outcomes in our transplant patients.
Alamanni and coworkers have contributed to this effort by examining the response of human venous endothelial cells in culture to hypothermic storage with four clinically relevant preservation solutions. Two of the solutions examined (Euro-Collins and St. Thomas) induced significant and irreversible injury to cultured vascular endothelial cells. Although not specifically examined by their study, these adverse effects may counterbalance the beneficial effects of these solutions on myocardial protection. These results are interesting and support the hypothesis that preservation solutions designed to protect cardiomyocytes may have deleterious effects on the vascular endothelium. Unfortunately, the independent contribution of each component in the solution on endothelial injury was not assessed. It is not clear from the study if a common variable within the damaging solutions induced endothelial dysfunction. This study evaluated the effects of the solutions on endothelial cell growth and morphological changes in vitro; the correlation with in vivo endothelial function is unclear. In addition, venous endothelial cells may react differently to preservation solutions than coronary arteriolar endothelial cells. Therefore, the clinical relevance of their findings will require animal testing.
Future work to identify a solution that protects both endothelial cells and cardiomyocytes from ischemic injury could be facilitated by the in vitro methods described by Alamanni and colleagues. Constituents or agents which are beneficial in vitro should be further tested in vivo, perhaps in a porcine model where both endothelial and myocardial function can be independently assessed in a cardiac allograft before storage, after prolonged storage, and most importantly after transplantation [2]. Enhancing preservation solutions with pharmacological supplements that block endothelium damage during storage may prevent endothelial dysfunction during reperfusion [3]. We are currently examining the ability of substrate-enhanced preservation solutions to restore both endothelial and myocardial function after prolonged storage in a preclinical porcine model. Novel protective strategies for organ preservation are certainly warranted, and targeting the vascular endothelium may prove to be an effective approach.
References
This article has been cited by other articles:
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  R.R. El-Akouri, C.A. Wranning, J. Molne, G. Kurlberg, and M. Brannstrom Pregnancy in transplanted mouse uterus after long-term cold ischaemic preservation Hum. Reprod., October 1, 2003; 18(10): 2024 - 2030. [Abstract] [Full Text] [PDF]
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