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Ann Thorac Surg 1996;62:1696-1697
© 1996 The Society of Thoracic Surgeons
DR GEORGE M. PALATIANOS (Athens, Greece): We have been using leukocyte-filtered blood cardioplegia for the last 2
years. We have seen that the patients in whom we use this type of cardioplegia have less arrhythmogenic activity postoperatively, less reperfusion ventricular fibrillation, and a smaller need for antiarrhythmics. Also we have noticed less use of inotropic agents postoperatively. These are our clinical observations. I would like to ask you to comment on this protective effect of the leukocyte-depleted cardioplegic solution against the postoperative arrhythmogenic activity.
My second question is referring to the results you showed us. How do you explain the lack of improved myocardial contractility of the hearts perfused with leukocyte-filtered cardioplegia in your experiments?
DR SCHMIDT: As far as improvement in any arrhythmogenic injury, I cannot explain that in particular other than saying that it is probably decreased injury overall. But I have no data to direct specifically at the issue of arrhythmias.
As far as the difference between global and regional function, we used the preload recruitable stroke work relationship to assess our global function. This was based on the conductance catheter, which allowed us to assess baseline function and then function after our interventions. We had hoped that with the comparison with baseline this technique would be sensitive enough to show a difference in global function relative to baseline; however, apparently the left ventricular reserve was adequate enough in both groups to attain. We did, however, add segment length crystals in the last 5 animals in the study. Because of the low numbers, we did not present that information today.
In the control group there was persistence of systolic lengthening (dyskinesis) in the ischemic region. In the leukocyte-depleted group there was decreased systolic segment shortening (hypokinesis), but it did contract. Global function greater than baseline was seen at the same time that systolic lengthening (dyskinesis) was seen in the control group, which is further evidence that our measurement of global function was not sensitive enough to detect regional injury. I think the injury is there, but our methods of detecting it were not sensitive enough.
DR GERALD D. BUCKBERG (Los Angeles, CA): In light of the previous paper on the use of l-arginine, evidently l-arginine by itself will produce nitric oxide and prevent the leukocyte adherence. Have you done any studies comparing your leukocyte filtration with l-arginine-type preservation to see if they were comparable or different?
DR SCHMIDT: We have not done that study. My suspicion would be that they may be complementary. We showed a difference in the leukocyte-depleted group from control, but there was still injury in the depleted group, and the addition of L-arginine may decrease that injury.
Related Article
Ann. Thorac. Surg. 1996 62: 1691-1696.
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