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Ann Thorac Surg 2002;73:1360-1361
© 2002 The Society of Thoracic Surgeons

Correspondence

Reply

James J. Gangemi, MDa, John A. Kern, MDa, Irving L. Kron, MDa, Curtis G. Tribble, MDa

a University of Virginia School of Medicine Lane Rd MR4 Building, Room 3116 Charlottesville, VA 22908 USA

e-mail: ctribble{at}virginia.edu

To the Editor

We very much appreciate the comments of Drs Miyamoto on our report [1], but we disagree with their conclusions. We will address some of their concerns regarding our study.

The hypothesis of our study was that retrograde perfusion of phenytoin would provide protection during prolonged periods of spinal cord ischemia, which is what our data demonstrated. Our objective was not to demonstrate complete cord protection. Furthermore, our laboratory uses a 45-minute aortic cross-clamping period because it results in consistent nearly complete paraplegia in our control groups [2, 3]. We have attempted shorter ischemic periods when establishing our control groups. However, these periods failed to produce persistent levels of paraplegia (unpublished data).

The first fundamental methodological flaw commented on by Drs Miyamoto concerned systemic phenytoin and whether enough time was allowed for it to cross the blood-brain barrier. Systemic phenytoin was infused only during the 45-minute ischemic period. We did not specifically evaluate the effects of prolonged systemic infusions of phenytoin beyond the 45-minute interval. Clearly the more highly concentrated systemic infusions of phenytoin had adverse effects. The purpose of this study was to demonstrate the effectiveness of localized delivery of a highly concentrated neuroprotective agent to the spinal cord without systemic effects of that agent. Ideally, this technique of retrograde venous perfusion avoids prolonged systemic exposure to and potential adverse effects of these agents.

In this study, we did not specifically measure spinal cord temperatures. Previous experiments in our laboratory using retrograde perfusion of a hypothermic solution (4°C) did not systemically cool the rabbits during a 45-minute infusion period [2]. This was further supported in experiments in our laboratory using the swine model of spinal cord ischemia where spinal cord temperatures were measured [4]. The temperature among all groups during the whole experiment, including that of the infusion solutions, was kept constant; therefore we did not measure spinal cord temperatures specifically. We cannot clearly state that the group given retrograde infusion of normal saline solution alone received protection as a result of decreased spinal cord temperatures. However, there was significant improvement in neurological function in the groups receiving retrograde phenytoin, a finding clearly indicating the protective effect of this agent on the spinal cord. This was quite different from the results with systemic phenytoin.

References

  1. Gangemi J.J., Kern J.A., Ross S.D., Shockey K.S., Kron I.L., Tribble C.G. Retrograde perfusion with a sodium channel antagonist provides ischemic spinal cord protection. Ann Thorac Surg 2000;69:1744-1749.[Abstract/Free Full Text]
  2. Parrino P.E., Kron I.L., Ross S.D., et al. Spinal cord protection during aortic cross-clamping using retrograde venous perfusion. Ann Thorac Surg 1999;67:1589-1595.[Abstract/Free Full Text]
  3. Gangemi J., Kern J., Kron I., Ross S., Shockey K., Tribble C. Retrograde venous perfusion of an NMDA receptor antagonist provides spinal cord protection during aortic cross-clamping. Surg Forum 1999;52:183-184.
  4. Ross S.D., Kern J.A., Gangemi J.J., et al. Hypothermic retrograde venous perfusion with adenosine cools the spinal cord and reduces the risk of paraplegia after thoracic aortic clamping. J Thorac Cardiovasc Surg 2000;119:588-595.[Abstract/Free Full Text]

Related Article

Is retrograde perfusion necessary for spinal cord protection?
Tadaomi-Alfonso Miyamoto and Koho-Julio Miyamoto
Ann. Thorac. Surg. 2002 73: 1360. [Extract] [Full Text] [PDF]




This Article
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John A. Kern
Irving L. Kron
Curtis G. Tribble
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