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Eur J Cardiothorac Surg 2004;25:1130
© 2004 Elsevier Science NL
Letter to the Editor |
Department of Cardiovascular Surgery,Marmara University School of Medicine,Istanbul, Turkey
Received 10 March 2004; accepted 15 March 2004.
* Corresponding author. Yakut 15/16, Atasehir, Istanbul 81120, Turkey. Tel.: +90-216-428-5777; fax: +90-216-325-2426
e-mail: drakgun{at}tnn.net
Key Words: Ischemia/reperfusion • Spinal cord • Aortic surgery
We thank Dr Lang-Lazdunski for his comments and concerns regarding our article [1]. We are familiar with the valuable research articles of Dr Lang-Lazdunski about spinal cord protection. As a matter of fact we cited his article in our manuscript [2]. However, we tried to compare the effects of two new agents which had not been studied previously with FK-5O6. Also there were no published articles comparing L-carnitine and azathioprine in spinal cord protection models. We think that this reflects the originality of our paper.
In our study, we did not entubate or ventilate any of the rats. We can conclude that the spinal cord injury was related to ischemia because if it were not so, the specimens of the sham group would not be fully normal and there would be necrotic changes in the histopathological examination of this group.
We agree that ketamine is a neuroprotective anesthetic agent. We think that ketamine anesthesia did not create a bias in our study since we anesthesized all the rats with ketamine. As you know, ketamine is one of the agents used for anesthesia in this type of animal models and its neuroprotective effects are not concerned so much [3,4].
The monitorization of the blood pressure of the proximal aorta was performed through a catheter placed in suprarenal aorta after midline laparotomy. Aortic cross clamp was placed just below the level of the catheterization site. Distal aortic pressure was measured through the femoral artery cannulation and there was no difficulty in the management of these procedures.
There are so many studies about the spinal cord ischemia reperfusion injury. Neuronal death in gray matter might be due to both necrosis and apoptosis. The results of our study suggest that 75% of neurons died due to apoptosis. This result may be due to the method that we used for detection of apoptosis in our study. The anti-PARP p85 fragment pAb was used for detection of apoptosis. PARP (human poly(ADP-ribose) polymerase) is a nuclear DNA-binding protein that detects DNA strand breaks. It is particularly important in DNA repair. Activation of the PARP is one of the earliest stages in apoptosis. Anti-PARP p85 fragment pAB specifically recognizes an 85 kDa band of PARP from the cells that are induced to undergo apoptosis. Thus, this antibody provides an early detection of apoptosis because cleavage of PARP occurs before DNA fragmentation that is detected by the use of TUNEL assays [5,6]. But further studies are required to confirm this result.
We did use the paragraph mentioned by Dr Lang-Lazdunski but as the information it contained was general knowledge about the pharmacological effects of FK-506, we did not think it was necessary to recitate Dr Lang-Lazdunski. Of course we should have and we are sorry for this oversight.
As a summary the conclusion of our study is not only the neuroprotective effects of FK-506 but also the neuroprotection by L-carnitine and azathioprine on spinal cord ischemia reperfusion injury with comparison.
References
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