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Ann Thorac Surg 2000;70:1449-1450
© 2000 The Society of Thoracic Surgeons
a The Heart Institute for Children, 4440 West 95th St, Oak Lawn, IL, USA 60463,
e-mail: bradallen{at}thic.com
To the Editor
I read with interest the paper by Lick and associates in which they cite using our technique of controlled pulmonary reperfusion to limit reperfusion damage in patients undergoing lung transplantation [1–4]. The authors are to be commended for applying the principles of controlled reperfusion to the clinical setting. Their excellent results confirm the validity of the experimental studies, and demonstrate that controlled reperfusion prevents a reperfusion injury in transplant patients.
My concern is that they have unnecessarily complicated the method of reperfusion by modifying our technique. Most problematic is that the authors leave the atrial clamp in place and the anastomosis open during the entire 10 minutes of controlled reperfusion. They collect the effluent (reperfusate) with a cell saver for reinfusion after it has been washed [1]. This necessitates temporarily removing 1,500 cc’s of blood from the patient in order to make the modified reperfusate. The authors state they do this to prevent hypotension from substances in the reperfusate solution, and to limit wash-out of active metabolites. I understand their concerns, but believe that this modification is completely unnecessary, increases potential problems, and make the procedure unduly complex.
In our laboratory studies, we took blood directly from the aorta, mixed it with a crystalloid solution using a cardioplegic mixer (BCD Blood Cardioplegia System, Sorin Biomedica, Arvada, CO), and then infused the modified blood solution into the transplanted lung (controlled reperfusion) for 10 minutes [2–4]. The atrial clamp was only left in place for approximately the first 60 seconds, to wash out the lung preservation solution to avoid electrolyte problems. This also allowed for deairing. The atrial clamp was then removed, so that blood from the aorta (modified reperfusate) immediately returned to the systemic circulation; this prevented hypovolemia and the need for blood transfusions. We used a clinically relevant large animal transplant model, without bypass, and had no episodes of hypotension or need for transfusions. In contrast, with their modification of first withdrawing 1,500 ccs of blood, the authors experienced both hypotension and increased need for transfusion.
Furthermore, we showed that the contralateral (nontransplanted) lung injury that occurs with uncontrolled reperfusion was completely prevented with controlled reperfusion. This indicates that wash-out of active inflammatory mediators is not a reason to modify our reperfusion protocol [2]. During the experimental studies, we initially worried that the high concentration of citrate in the reperfusate solution might cause hyocalcemia and hypotension; however, no animal became hypotensive. Nevertheless, we recommend that calcium be available in the event hypotension occurs during reperfusion. We agree with Lick and associates that the modified reperfusate should be infused at a pressure of 20 mm Hg. In contrast to our early studies, we confirmed this in an article just published in this journal [4]. Lastly, based on our recent work in the heart, we believe that prostaglandins should probably replace nitroglycerine in the modified reperfusate solution [5].
I again congratulate the authors and their coworkers on their pioneering clinical study. Now that the experimental findings have been confirmed clinically, I hope that they, and others, will undertake the necessary larger randomized trial.
References
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  B. S Allen The role of leukodepletion in limiting ischemia/reperfusion damage in the heart, lung and lower extremity Perfusion, March 1, 2002; 17(2_suppl): 11 - 22. [Abstract] [PDF]
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G. A Ortolano, G. S Aldea, K. Lilly, P. O'Gara, J. D Alkon, F. Madera, T. Murad, C. P Altenbern, C. S Tritt, A. Capetandes, et al. A review of leukofiltration in cardiac surgery: the time course of reperfusion injury may facilitate study design of anti-inflammatory effects Perfusion, March 1, 2002; 17(2_suppl): 53 - 62. [Abstract] [PDF]
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