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Ann Thorac Surg 1996;62:1300
© 1996 The Society of Thoracic Surgeons
DR ANDREW S. WECHSLER (Richmond, VA): I enjoyed your paper very much. Did you do any experiments where you gave your protective agent without any ischemia just to see what the effect of the agent itself was? It strikes me that there may be some osmotic effect or something other than adhesion receptor blockage that might be working.
DR MIURA: In this experiment we used a 30 mg/L concentration because it seemed likely to have blocked the function of selectin but did not cause obvious cardiac and vascular side effects.
DR WECHSLER: What happens if you give just the fucoidin alone, with no ischemia?
DR MIURA: There is almost no effect: no cardiac effect and no vascular effect.
DR RICHARD M. ENGELMAN (Springfield, MA): The obvious finding here is a marked increase in coronary blood flow, isn't that the case? And could that not be an explanation for your increase in myocardial oxygen consumption and even an increase somewhat in your myocardial contractility?
DR MIURA: I am not sure of the exact reason for the better recovery of left ventricular function.
DR ENGELMAN: I was just commenting on the marked increase in coronary flow, which could also explain some of the other physiologic findings that you uncovered. But you did indicate that the fucoidin does not have a coronary vasodilating effect in and of itself. Is that what you found?
DR MIURA: Yes. In the previous study we used leukocyte depletion instead of the fucoidin infusion. In that case there was a marked increase of the coronary blood flow after reperfusion compared with the control group. I think the prevention of the leukocyte function had some effect on the coronary vasodilation during the reperfusion period.
DR MEHMET C. OZ (New York, NY): We have used P-selectin knock-out mice and have obtained results very similar to yours. In that experimental model we have taken mice that do not have the P-selectin upregulation ability and transplanted those hearts, and so I do believe that it could work by that mechanism. But my question is, why would you think that fucoidin works solely by that mechanism, and how did it become evident that fucoidin blocked selectin receptors and endothelial cells?
DR MIURA: I think that the structure of the fucoidin is almost the same as the structure of the ligand for P-selectin, so the saturation of the P-selectin itself is a mechanism that prevents function of the P-selectin.
Related Article
Ann. Thorac. Surg. 1996 62: 1295-1300.
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