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Ann Thorac Surg 1999;67:25-26
© 1999 The Society of Thoracic Surgeons
Discussion
DR EDWARD D. VERRIER (Seattle, WA): This brings me back to my 3 years in the laboratory of Julian Hoffman. Julian Hoffman was one of the foremost coronary blood flow physiologists of our era. This is a very difficult model, and the concept that you completely lose all autoregulation of coronary blood flow is a difficult concept. Normally, you can drop the coronary perfusion pressure of a dog or pig even down to about 40 mm Hg, and you maintain a constant flow (ie, autoregulate). At about 40 mm Hg, flow drops off, and the pressure–flow relation becomes linear. The curves that you show are at minimal resistance, so that pressure and flow follow when the pressure goes up or down. And that is a very difficult concept for a coronary blood flow physiologist to understand, and I think that the data would have to be very, very carefully looked at.
If it is true, it has implications, obviously, for the donor pool.
What is it that you postulate is released by the brain that affects coronary vascular resistance to this degree, isolated from effects on other beds? Because that is what it would have to be if it is going to be uncoupled like this. You are postulating something from the brain that ends up in the heart that drops coronary vascular resistance so that it is at a minimal level, so that it becomes a pressure-dependent bed.
DR SZABÓ: Thank you very much for your question. It is true that in isolated heart models, and this model is also a type of isolated heart model, the coronary autoregulation is at least partially lost. This may be one explanation why we found a linear relation between coronary pressure and flow at a pressure from 40 to 100 mm Hg. However, overlooking the published data, a linear relation between coronary pressure and flow was also found below a "critical" pressure of 60 to 80 mm Hg in in situ ejecting heart models. This linearity of the coronary perfusion pressure–flow relation in the lower pressure range may have significance in the brain-dead organ donor, where systemic vascular resistance is decreased owing to a loss of sympathetic vasomotor tone, which consequtively leads to a decrease in coronary perfusion pressure. One can expect that even in ejecting heart models, the coronary pressure–flow relation becomes linear at lower perfusion pressures after brain death. At the moment when coronary autoregulation is exhausted, it is possible that myocardial contractility also decreases.
DR VERRIER: If you postulate that the function is tied into this, then you almost have to postulate that there is ischemia (ie, that is why flow drops). So if you increase perfusion, you would then recover the function. One thing that would be interesting is if you used radioactive microspheres or something that you could get at the transmural distribution of blood flow and see if you really can document that there is some diminution of flow in the subendocardium.
DR SZABÓ: There are many possible explanations for contractility–perfusion matching. One of them may be myocardial ischemia. We measured myocardial oxygen consumption and lactate release from the heart, and we did not see any differences before and after brain death and in connection with the changes of coronary perfusion pressure. Therefore, I think that cardiac depression is unlikely to be caused by ischemia.
Another possible mechanism may be the so-called garden-hose effect, which is described in isolated hearts. It postulates that an increase in coronary perfusion pressure results in an increased intramural myocardial stretch and, subsequently, contractility. Even if the garden-hose effect was not observed in normal and hypertensive ejecting hearts, it probably also has significance in situ in the lower pressure range with exhausted autoregulation. Therefore, the changes in myocardial contractility after brain death can be seen as a result of the garden-hose effect.
DR MAGOVERN: One other observation. The neurosurgeons at our hospital have a model of subarachnoid hemorrhage, which is a different model, and they have looked at myocardial function in that model. There is evidence, both electrocardiographic and also transesophageal echocardiographic, of regional cardiac dysfunction, which looks identical to a myocardial infarction, at least by regional function changes. It is presumably due to changes in sympathetic outflow in response to the cerebral injury. There are models of myocardial ischemia that are out there, not for this particular model, but for a subarachnoid hemorrhage model.
DR SZABÓ: Thank you for your comment.
DR VERRIER: I think it is an excellent study as a prelim because I think all of us have had patients who are 18 or 20 years old who have what would appear to be a minimal myocardial injury, or whatever, and you look at your echocardiogram, and there is marked myocardial depression, and you are making a decision then as to whether to use this heart that otherwise ought to be normal. So this line of investigation is clearly important, and there are, as Jim said, a number of models looking at whether there are myocardial depressant factors that are elaborated.
Related Article
Ann. Thorac. Surg. 1999 67: 18-25.
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