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Ann Thorac Surg 1996;61:40-41
© 1996 The Society of Thoracic Surgeons
DR GUO-WEI HE (Portland, OR): This has been a nice presentation. I have three questions for you. The first question is, what is the final concentration of endothelin-1 in the perfused blood after bolus injection, and is it clinically relevant? This is very important because we know that the plasma concentration of endothelin-1 is very low. Would you like to comment on the clinical relevance of your study?
The second question regards the source of endothelin-1 release. There are two sources to consider. First, after cardiopulmonary bypass, the elevated plasma concentration of endothelin-1 could be due to release from the systemic circulation. Second, as you hypothesized, endothelin-1 could be directly derived from the coronary circulation rather than from the systemic circulation. Your hypothesis is based on the second point, and I appreciate it. However, your results rejected this hypothesis because the endothelin-1 levels in coronary sinus blood were constant. This does not, however, exclude the possibility that the endothelin-1 plasma concentration is elevated after cardiopulmonary bypass, as already measured in patients by others. This elevated endothelin-1 level may be related to the release from the endothelium in the systemic circulation. Therefore, one must realize that because your studies on the isolated heart model did not look at endothelin-1 release from the endothelium in the systemic circulation as the effect of cardiopulmonary bypass, your results cannot be simply applied to the clinical setting, in which, unlike in your study, the absolute concentration of endothelin-1 is elevated after cardiopulmonary bypass. In other words, your conclusion-that during ischemia/reperfusion, the effect of endothelin-1 dominates-is made only because the production of EDNO is impaired, which may not be true because an elevated plasma concentration of endothelin-1, due to the release from the systemic circulation in response to cardiopulmonary bypass, may also affect myocardial perfusion and heart function.
The third question is that in your study, the endothelin-1 level was constant at 30 minutes of ischemia/reperfusion but the total ischemia/reperfusion time was 2 hours, as indicated in the abstract. Why was the endothelin-1 level from the coronary sinus blood not measured at the end of ischemia/reperfusion, that is, at 2 hours? At that time, the endothelin-1 level may be elevated.
DR JOHN W. HAMMON JR (Winston-Salem, NC): That was a very nice report. I was concerned about one methodologic point. In our laboratory, we have been unable to get very dramatic responses using l-arginine to control reperfusion injury unless we pretreat the animals before the ischemic period. Do you have any comments?
DR HIRAMATSU: Thank you very much for your comments.
To the first discussant, the final endothelin-1 levels are 2.2 to 2.5 pmol/L, almost the same as just after reperfusion. Our original expectation was that there would be increased endothelin-1 levels after reperfusion, but our model is not of hypoxia, it is of anoxic hypothermic ischemia. There is a difference between hypoxia and anoxia. We think that this may be the reason why the endothelin level is constant before and after ischemia.
We do not have any direct evidence to answer the question of whether the endothelin-1 originated from the coronary circulation, but we measured the endothelin-1 level from the coronary sinus plasma.
As you pointed out, the functional recovery of the combined fourth group is a little bit lower than the control level, but there is no statistically significant difference. We assume that the functional recovery of the combined l-arginine and endothelin group belongs to the control level.
DR LEVITSKY: Doctor Mayer, perhaps you could help him with the last question.
DR MAYER: The last question addressed the issue of whether you need to pretreat the hearts with l-arginine or somehow enhance the capability of producing nitric oxide. Preischemic treatment has not been necessary in our experience in this model; perhaps some interspecies differences or some other factor explains why your results are different from ours. I can say that the l-arginine effect is not trivial, and it is very impressive the way these hearts look after they have been given l-arginine for the first 15 or 20 minutes of reperfusion. You can look at the exterior surface of the heart and say that this is an l-arginine-treated heart. This is not a subtle difference in what the coronary arteries look like and what the perfusion of the myocardium looks like.
This article has been cited by other articles:
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  O. Pitkanen, M. Niskanen, S. Rehnberg, M. Hippelainen, and M. Hynynen Intra-institutional prediction of outcome after cardiac surgery: comparison between a locally derived model and the EuroSCORE Eur. J. Cardiothorac. Surg., December 1, 2000; 18(6): 703 - 710. [Abstract] [Full Text] [PDF]
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