| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Ann Thorac Surg 1996;62:240-241
© 1996 The Society of Thoracic Surgeons
DR SHAF KESHAVJEE (Toronto, Ont, Canada): I congratulate Dr Van Raemdonck and associates on a very well thought-out, nicely planned, and carefully analyzed experiment. I appreciate the opportunity to have reviewed the manuscript before this.
Those of us who are interested in the study of non–heart-beating donors have come to realize that all non–heart-beating donors are not the same, and that factors occurring both before and after death can have significant impact on posttransplantation lung function. Clearly further careful study is required of non–heart-beating donors to identify the critical factors that will allow us to predict which lungs can be used for transplantation, and this study is one important first step along that line.
I have two questions. First, do you have any functional assessment data on the groups that you studied in this study to correlate your metabolic preservation with predicted postreperfusion lung function? Second, why did you choose to use Krebs-Henseleit as the flush control in this study?
DR VAN RAEMDONCK: Thank you, Dr Keshavjee. We appreciate your comments.
Indeed, not all non–heart-beating donors can be categorized in the same group. In a recent symposium held last year in Maastricht, the Netherlands [1], four groups of non–heart-beating donors were categorized, from the totally uncontrolled donor up to the well-controlled non–heart-beating donor, and indeed there will be a big difference in posttransplantation lung function between all these groups of non–heart-beating donors depending on the quality of resuscitation and the length of warm ischemia.
To answer your first question, yes, we are looking at functional assessment of lungs preserved after circulatory arrest in the way as presented here today using an isolated ex vivo closed-circuit rabbit reperfusion model, but at the moment we are in the process of analyzing our results. We can only say that we can confirm the results in the literature that indeed postmortem ventilation and inflation can prolong lung viability, and this is reflected already by a delay in the onset of lung edema during delayed pulmonary flush up to 6 hours after circulatory arrest.
To answer your second question, why we used Krebs-Henseleit solution, Krebs-Henseleit solution is a widely used bicarbonate buffer, well known in the older literature of lung preservation as well as heart preservation. The composition of electrolytes in Krebs-Henseleit solution is not very different from low-potassium dextran, except that there is no dextran in this solution. It is an extracellular type of solution, and we are very familiar with this solution in our laboratory.
DR THOMAS M. EGAN (Chapel Hill, NC): I have one quick question. We, too, thought we would be able to preserve ATP levels and viability by ventilating dog lungs with cold air and found that when we put a temperature probe in the lung we could not cool a lung that way. Did you measure the temperature in your rabbit lungs that you ventilated cold?
DR VAN RAEMDONCK: Yes, we measured lung temperatures in these groups, and this will be presented tomorrow in the poster session [2]. I can now say that ventilation with cooled air will not decrease lung core temperature or lung surface temperature but will only influence the endobronchial temperature. So we did not expect to have any more benefit in delaying ATP catabolism from ventilation with cooled air when compared with ventilation with room air at room temperature.
DR ANDREA M. D'ARMINI (Pavia, Italy): Congratulations on the work you conducted; that was a very nice report.
I have two questions. The first regards the levels of HYP, the main catabolite of ATP, which are very low at time 0. At 2 and 4 hours after sacrifice you have similar levels in two of your study groups: deflated and ventilated with 100% oxygen. Do you have an explanation for this, because in one of our experiments, at the University of North Carolina, on non–heart-beating lung donors, we found that the levels of HYP in lungs ventilated with 100% oxygen were much lower than those in nonventilated lungs. This appears to us to be an important demonstration that supplying nonperfused lungs with oxygen delays the catabolism of adenine nucleotides.
The second question is about topical cooling. I agree that this is an efficient method for slowing down the adenine nucleotide catabolism in cadaveric lungs. However, I do not believe that in a possible clinical setting in which these donors would be used, topical cooling is very practical. In an emergency room situation, prompt mechanical ventilation of this cadaver donor with 100% oxygen would appear to be the only feasible approach.
DR VAN RAEMDONCK: Hypoxanthine levels in lungs ventilated with room air were significantly lower at 2 and 4 hours when compared with lungs left deflated. We compared levels in lungs ventilated with pure oxygen versus lungs ventilated with room air and we did not found any significant differences in ATP, TAN, and HYP levels, although at 24 hours there was a trend that ventilation with 100% oxygen created higher HYP levels when compared with ventilation with room air.
To answer your second question, how to translate all this into the emergency room and see how non–heart-beating donors can be cooled after unsuccessful resuscitation, this will also be presented tomorrow, but we can say that topical cooling by submerging the cadaver in ice will take about 4 hours to get the lung temperature to less than 10°C. Also, ventilation with cooled air, as explained previously, will not be able to cool lung temperature. We therefore think it will not be realistic to decrease lung temperature after circulatory arrest in the emergency room by these methods. We believe that other methods, like in situ cold pulmonary flush through in-dwelling arterial catheters or cooling on extracorporeal bypass, will be necessary to cool these lungs.
References
| ||||||||||||||||||||||||||||||||||||||||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
| ANN THORAC SURG | ASIAN CARDIOVASC THORAC ANN | EUR J CARDIOTHORAC SURG |
| J THORAC CARDIOVASC SURG | ICVTS | ALL CTSNet JOURNALS |
