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Eur J Cardiothorac Surg 2006;30:415
© 2006 Elsevier Science NL
Letter to the Editor |
Department of Paediatric Cardiothoracic Surgery, Royal Hospital for Sick Children, Dalnair Street, Glasgow G3 8SJ, UK
Received 15 March 2006; accepted 5 May 2006.
* Corresponding author. Tel.: +44 141 201 0251; fax: +44 141 201 9204. (Email: mrmhanif{at}doctors.net.uk).
Key Words: Lung transplantation Seldinafil Preservation
We read with interest the recent article by Stehpan and colleagues [1] titled Sildenafil extends survival and graft function in a large animal lung transplantation model. We appreciate the effort and hard work of the authors on this topic. Indeed large animal model studies are notorious for being time and labor intensive and require approval from statutory authorities.
Lung transplantation is an established therapy for end-stage lung disease [2]. Although improving survival figures in lung transplantation remain inferior to that achieved with other organ transplantation. One major area of concern is that of significant ischemiareperfusion injury leading to allograft dysfunction. Therefore, any laboratory work that can translate into improved graft function in the clinical setting would be most welcome. Interestingly, sildenafil is finding more and more uses as a selective phosphodiesterase inhibitor. Some work has focused on its role in pulmonary hypertension. Recent work by Dark's group [3] in Newcastle upon Tyne has focused on deleterious effects of brain-stem death on donor lungs in the animal model. This brain-stem death induced injury to the lung appears to be a major determinant of its function following transplantation. Therefore, we would welcome further studies of sildenafil in the brain-stem death damaged donor lungs.
Footnotes
The authors of the original paper [1] were invited to comment on this Letter to the Editor but declined the offer.
References
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