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Eur J Cardiothorac Surg 2000;18:731
© 2000 Elsevier Science NL

Letter to the Editor

Reply to Abdul-Khaliq et al.

Paediatric Cardiac Surgery, Great Ormond Street Hospital for Children, London, WC1N 3JH, UK

Received 10 July 2000; accepted 11 September 2000.

Corresponding author. Tel.: +44-23-8079-6241; fax: +44-23-8079-8508
e-mail: stephenlangley{at}dial.pipex.com

I was very interested to read the comments of Dr Abdul-Khaliq and associates and to read of the results from their own study. Firstly I would like to try and allay concerns regarding the methodology used in our study. The markers of cerebral injury used were recovery of cerebral blood flow (CBF) and cerebral metabolism (CMRO₂). We believe that these are important surrogates of brain injury. The reduction in CMRO₂ that follows a period of deep hypothermic circulatory arrest (DHCA) has been regarded by some authors as a marker for neuronal injury for some time now as CMRO₂ recovers normally after hypothermic bypass when DHCA is not used. More recently however in a study using electron microscopy we have been able to demonstrate a correlation between the recovery of CMRO₂ and of cerebral ultrastructure [1]. In the control group in our study 60 min of DHCA followed by 60 min of rewarming resulted in a significant impairment in the recovery of both CBF and CMRO₂. This response to DHCA was attenuated by preoperative methylprednisolone (30 mg/kg) given at 8 and 2 h preoperatively. I believe that the conclusions as given in our paper are fully justified.

Regarding the study of Dr Abdul-Khaliq and associates there are a number of different reasons which might explain their results. Firstly although methylprednisolone was given in the same dose (30 mg/kg) as in our study I am not sure of either the route of administration, the number of doses or the timing of the doses. In our own study the timing of the doses was based on evidence that de novo protein synthesis is involved in the cerebroprotective effect of corticosteroids [2]. Secondly the duration of the circulatory arrest period was unfortunately not specified. Finally failure to adequately perfusion fix the brain prior to histological examination with a solution such as that described by Karnovsky [3] can lead to artefactual areas of damage. The suggestion from the letter is that the brains were not perfusion fixed and this as another possible reason for the results obtained. Nevertheless I would concur wholeheartedly with Dr Abdul-Khaliq that further studies in this area are warranted prior to routine use in neonates.

References

1. Langley S.M., Chai P.J., Miller S.E., Mault J.R., Jaggers J.J., Tsui S.S., Lodge A.J., Lefurgey A., Ungerleider R.M. Intermittent perfusion protects the brain during deep hypothermic circulatory arrest. Ann Thorac Surg 1999;68:4-13.[Abstract/Free Full Text]
2. Temesvari P., Joo F., Koltai M., Eck E., Adam G., Siklos L., Boda D. Cerebroprotective effect of dexamethasone by increasing the tolerance to hypoxia and preventing brain oedema in newborn piglets with experimental pneumothorax. Neurosci Lett 1984;49:87-92.[Medline]
3. Karnovsky M.J. A formaldehyde-glutaraldehyde fixative of high osmolality for use inelectron microscopy. J Cell Biol 1965(27):137A.

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