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Ann Thorac Surg 2000;69:716
© 2000 The Society of Thoracic Surgeons

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Discussion

Discussion

DR W. STEVES RING (Dallas, TX): Dr Goldberg, this was really a very nice, clean study and very well presented. What is your concept of the role of the sodium hydrogen ion exchange mechanism as a contributor to the contractile dysfunction versus other effects on the contractile proteins?

DR GOLDBERG: Well, as part of the transduction pathway for an endothelin-mediated response, I feel like there is a very strong association between the sodium hydrogen exchanger and contractility. Now, these studies were performed on isolated myocytes, devoid of any other neurohormonal or vascular changes as with an in vivo model. At least in the isolated myocytes, the sodium hydrogen exchanger appeared to be very influential in myocyte contractility and contractile performance.

DR PAUL A. KURLANSKY (Miami Beach, FL): I wanted to first congratulate you on a very elegant study. It was perhaps my own failing in understanding the diagram that you presented at the end, but as I understood your data, inhibition of either PKC or of sodium hydrogen exchange completely blocked the contractile response, therefore, either one is completely necessary in order, in this model, to have the contractile response. However, in your diagram, it seemed as though there were independent pathways that were not necessarily reliant one upon the other, ie, they were in parallel, as it were, rather than in series, but the data would seem to indicate that they are both components, essential components, because either one by itself completely knocked out the response. I was wondering if you could comment on that.

DR GOLDBERG: That is a very good point. Our initial theory was that these two pathways are actually in series. As demonstrated when we combined the two inhibitors, we found that there was no additional increase, or a negative effect on contractility. There are certainly other factors that are involved in this transduction pathway that we are currently investigating, and I do not have the data to support that they are actually parallel. It is suggested that the endothelin response is mediated both through a series and a parallel transduction pathway.

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