ATS
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
 QUICK SEARCH:   [advanced]


     


This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Search for Related Content
Related Collections
Right arrowRelated Article

Ann Thorac Surg 1997;63:26-27
© 1997 The Society of Thoracic Surgeons


Discussion

Discussion

See also page 20.

DR RALPH J. DAMIANO (Hershey, PA):

Doctor Murphy, I congratulate you on a beautiful presentation of very interesting data. I have several questions and would like your opinion on the clinical relevance of your findings.

First, have you looked at the time course of recovery? From a clinical standpoint, this would be very important. Is this a prolonged impairment of vasoreactivity or is this something that 6 or 12 hours later has resolved completely?

My second question is: Have you looked further at more clinically significant physiologic correlates of your findings? Have you found in any other models a real difference in postreperfusion blood flow that may correlate with some of the isolated vessel findings?

You concluded by speculating that by altering the cardioplegic solution, one may decrease the late incidence of transplant vasculopathy. But has there really been a difference in late transplant vasculopathy in hearts preserved with University of Wisconsin solution, which is your preferred solution, as opposed to some of the solutions you have shown to be not quite as beneficial?

DR MURPHY:

The first question concerned the late effects of microvascular impairment and whether this is a prolonged effect with the endothelium-dependent response. It is prolonged with these vessels. We found that several hours afterward, after we had harvested these vessels and put them in our microvessel preparation, we still saw this impairment in the response, and it did not recover. The literature has been able to show us that this contributes to the myocardial stunning seen after cardiac operations, which sometimes can be prolonged up to 7 days, and this may be due to the microvascular dysfunction.

The second question was whether we have any other studies, or if there are any in the literature, that might correlate clinically to the right ventricular flow.

DR DAMIANO:

Or using some other more clinically relevant physiologic correlates of this finding. Have you looked at postreperfusion blood flow, for example, using a microsphere technique?

DR MURPHY:

We have a study ongoing in our laboratory examining cardioplegia flow with microspheres. Preliminary results show that right ventricular blood flow is two thirds of the left ventricular blood flow.

DR DAMIANO:

You have implied that there was a beneficial effect of University of Wisconsin solution, and you suggested that this might decrease late transplant vasculopathy. In the literature, there does not appear to be much to suggest that the incidence of transplant vasculopathy is very related to the different preservation solutions.

DR MURPHY:

There is nothing in the literature to date that examines whether University of Wisconsin solution makes a difference in terms of development of transplant vasculopathy. I do believe that the preservation of the endothelium-dependent function can alter the course of development of transplant vasculopathy.

DR SIDNEY LEVITSKY (Boston, MA):

I have two questions for you. The essence of your study is that there are differences between the right and left coronary circulations in the coronary microvascular endothelial reactivity response to acellular cardioplegia. You also have stated that Dr Frank Sellke has shown that endothelial reactivity could be eliminated by blood perfusion. Thus, the first question is, can blood cardioplegia alter the discrepancy between the right and left ventricles? The follow-up question is, what is the physiologic or teleologic explanation for this observed difference in endothelial reactivity between the ventricles?

DR MURPHY:

Blood added to crystalloid cardioplegia, as Dr Sellke demonstrated, can improve the microvascular reactivity.

DR LEVITSKY:

What is your hypothesis regarding the difference?

DR MURPHY:

The difference may be related to the distribution of cardioplegia to the right and left ventricles. The literature has shown that a greater amount of cardioplegia is distributed to the left ventricle than the right under hypothermic conditions. Thus, the greater cardioplegic distribution to the left ventricle results in the better microvascular reactivity.


Related Article

Coronary Microvascular Reactivity After Ischemic Cold Storage and Reperfusion
Charles O. Murphy, Pan-Chih, John Parker Gott, and Robert A. Guyton
Ann. Thorac. Surg. 1997 63: 20-27. [Abstract] [Full Text]




This Article
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Alert me to new issues of the journal
Right arrow Add to Personal Folders
Right arrow Download to citation manager
Right arrow Permission Requests
Citing Articles
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Search for Related Content
Related Collections
Right arrowRelated Article


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