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Ann Thorac Surg 1996;62:61-62
© 1996 The Society of Thoracic Surgeons
DR DAVID A. FULLERTON (Denver, CO): Doctor Mauney, I compliment you on a beautiful presentation. I think that you and your colleagues at the University of Virginia continue to lead the way in trying to fine-tune the mechanisms of organ procurement and organ protection, and we are all waiting for this to become an elective operation. So I compliment you in that regard.
I was wondering if I could get you to speculate on a couple of things. You have a very elegant setup, and so I suspect that you may have thought about or even initiated the experiments to do a couple of things. I must admit that I found the function of your cardiac groups to be significantly better than I would have anticipated; you clearly have a technique here to study some of the mechanisms of myocardial preconditioning. Have you had an opportunity to try to make these hypoxic and reperfused groups function even more closely to controls? And if so, might you be able to speculate on whether preconditioning influences infarction, which I suspect you are probably able to produce in this model, versus stunning?
I found it ironic that the lung was so resilient. As we all know, it is very difficult to procure lungs, primarily because the lung is so sensitive to a variety of injuries and therefore by the time an organ donor becomes available, the lung is frequently dysfunctional, yet you have shown in this model that the lung was more resistant than the heart, at least to this specific injury. I know you speculated a bit on it; I was curious if you might have had an opportunity to look at some of the mechanisms involved in that as well.
DR MAUNEY: Thank you for those comments, Dr Fullerton. With regard to your first question about the relative lack of injury in the 30-minute warm ischemia group compared with both hypoxic arrested groups, previous authors using a similar protocol of isolated, blood-perfused rabbit hearts undergoing 30 minutes of global warm ischemia reported recovery of function in the range of 50% to 70% of baseline. Our 30-minute warm ischemia hearts displayed left ventricular developed pressures of approximately 60% compared with controls. Therefore we were confident that we were seeing an appropriate degree of injury in the 30-minute warm ischemia group.
With regard to your second question about additional studies of preconditioning and stunning in this model, yes, we have looked into this. We believe strongly in the clinical feasibility of using allografts from non–heart-beating donors and believe that preconditioning and modulating myocardial stunning will be important interventions in making this a reality. We have already carried out experiments demonstrating improved recovery of function in this same model with prearrest doses of the 
-agonist phenylephrine and look forward to presenting these data in the near future. Most likely, myocardial stunning is present in this model of injury, as we have reproducibly seen a gradual improvement in ventricular function during and after the 45-minute reperfusion period. We did not look at any objective measurements of myocardial infarction in this model, but these could be performed in future studies to better understand if the reduced function is due to stunning or infarction.
The lack of injury in the experimental lungs undergoing either 30 minutes of warm ischemia or hypoxic arrest followed by 20 minutes of warm ischemia surprised us as well. I think the differences between our model and other isolated lung preservation models are at least partially responsible. The overwhelming majority of isolated lung preservation studies have at least 4 hours of cold storage before reperfusion, which can result in a significant reperfusion injury. We were intent on isolating the effects of prearrest hypoxic perfusion and postarrest warm ischemia on lung function. Therefore we intentionally reperfused these organs immediately after the experimental protocol without any cold storage. Future studies looking at cold storage after non–heart-beating donation would help confirm this hypothesis.
DR FRANCIS ROBICSEK (Charlotte, NC): This very elegant study reinforces two old postulates: (1) ischemia is bad for the heart and (2) ischemia is even worse for the working heart. This report paints somewhat of a bleak picture of the possibility of transplanting hearts removed from non–heart-beating donors. However, things may be not that bad. In the early 1970s we published observations on hearts removed from humans just deceased from noncardiac conditions who were rushed down to the morgue, after which the heart was removed, resuscitated, and converted into a functioning heart-lung preparation. Those hearts beat very happily for several hours with normal hemodynamic parameters. So despite these somewhat pessimistic findings, I would not drop the idea of cadaveric heart transplantation.
DR MAUNEY: Thank you, Dr Robiscek. We would certainly agree that clinical application of non–heart-beating donors for thoracic transplantation is possible but that additional large-animal survival studies are needed to determine the optimal prearrest and postarrest resuscitation techniques.
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