EJCTS Click here for details of sales representative
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

This Article
Right arrow Full Text (PDF)
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 Articles by Isbir, C. S.
Right arrow Articles by Ak, K.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Isbir, C. S.
Right arrow Articles by Ak, K.
Related Collections
Right arrow Great vessels

Eur J Cardiothorac Surg 2003;24:853
© 2003 Elsevier Science NL

Letter to the Editor

Reply to Toumpoulis

C. Selim Isbir*, Koray Ak

Department of Cardiovascular Surgery, Marmara University School of Medicine, Istanbul, Turkey

Received 7 August 2003; accepted 10 August 2003.

* Corresponding author. Avukat Sureyya Agaoglu sokak No: 4b D: 17, Nisantasi, Istanbul 80200, Turkey. Fax: +90-212-6351959
e-mail: isbir{at}yahoo.com

Key Words: Ischemic preconditioning • Aortic surgery

We thank Dr Toumpoulis for his nice comments regarding our article entitled ‘Ischemic preconditioning and nicotinamide in spinal cord protection in an experimental model of transient aortic occlusion’. He highlights the important point that keeping the blood pressure above 100 mmHg reduces the postoperative neurological dysfunction during the aortic occlusion [1]. We concur completely that hypotension should be avoided during aortic occlusion. This might reduce the collateral circulation. In our model, the tail artery was cannulated for distal aortic pressure. Blood pressure dropped from 80–90 to 10–20 mmHg after cross-clamping. However, our aim was to confirm that cross-clamping was complete. Heartbeats were around 180–190. We did not find any correlation with blood pressure and neurological scoring. However, we discarded four animals that had hypotension due to hemorrhage.

With regard to the comments for improvement in paraplegia from 24 to 48 h, as stated in our article we think that apoptosis might be the underlying mechanism. The necrotic cells in light microscopy might be apoptotic and terminal damage might not occur. We measured the apoptotic cells in 48 h. Another study comparing the histological changes and the number of apoptotic cells at 24 and 48 h of the experiment should be undertaken to explain this finding. However, we did not focus on the mechanism for reduced apoptotic cell death by ischemic preconditioning (IPC) in our study. Recent studies have shown the importance of inhibitors of apoptosis (IAP) following spinal cord injury [2].

Another point that has been raised is the duration of IPC. This has different time scales in various studies [3,4]. We believe that at least 5 min of ischemia should be present for the protective effect of IPC.

In conclusion, IPC is a promising method in spinal protection and further studies are needed to explain the underlying mechanism.

References

  1. Toumpoulis I.K., Anagnostopoulos C.E., Drossos G.E., Malamou-Mitsi V.D., Pappa L.S., Katritsis D.G. Early ischemic preconditioning without hypotension prevents spinal cord injury caused by descending thoracic aortic occlusion. J Thorac Cardiovasc Surg 2003;125:1030-1036.[Abstract/Free Full Text]
  2. Keane R.W., Kraydieh S., Lotocki G., Bethea J.R., Krajewski S., Reed J.C., Dietrich D. Apoptotic and anti-apoptotic mechanisms following spinal cord injury. J Neuropathol Exp Neurol 2001;60:422-429.[Medline]
  3. Zvara D.A., Colonna D.M., Deal D.D., Vernon J.C., Gowda M., Lundell J.C. Ischemic preconditioning reduces neurologic injury in a rat model of spinal cord ischemia. Ann Thorac Surg 1999;68:874-880.[Abstract/Free Full Text]
  4. Caparrelli D.J., Cattaneo S.M., Bethea B.T., Shake J.G., Eberhart C., Blue M.E., Marban E., Johnston M.V., Baumgartner W.A., Gott V.L. Pharmacological preconditioning ameliorates neurological injury in a model of spinal cord ischemia. Ann Thorac Surg 2002;74:838-844.[Abstract/Free Full Text]




This Article
Right arrow Full Text (PDF)
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 Articles by Isbir, C. S.
Right arrow Articles by Ak, K.
Right arrow Search for Related Content
PubMed
Right arrow Articles by Isbir, C. S.
Right arrow Articles by Ak, K.
Related Collections
Right arrow Great vessels

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