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apoptosis andischaemic neuronaldeath,whereas anincrease in the pro-apoptotic protein Bax has been shown to promote cell death by caspase activation. Our observation that mild hypothermia increases the Bcl-2/Bax ratio following DHCA is consistent with cerebral protection via decreased apoptotic cell death. DrSakuraiisthinkingahead—given that there isprotection, what cell types would be affected? In the experiments reported, we did not attempt to determine whether neurons were the primary site of brain injury but focussed on whether hypothermia can decrease the injury[2]. The extensive literature on this subject shows that cardiopulmonary bypass and deep hypothermic circulatory arrest induce neuronal injury. In our publication, we discussed neuronal injury; however, our data did not distinguish among the different cell types. In an identical experimental protocol, we used the terminal dUTP nick-end labelling to detect apoptotic cells (TUNEL) stain on the perfused piglet brain following 6 h of post-bypass recovery (unpublished data). We observed that there were increased numbers of TUNEL-positive cells following DHCA but, because of the short recovery period, the numbers were too low to allow testing for an effect of hypothermia. While TUNEL cannot distinguish apoptosis from necrosis, it is a valuable marker of neuronal cell damage. Experiments using 12-h recovery periods, where the number of TUNEL-staining cells is substantially higher, are in progress. TUNEL measurements are being combined in our long-term experiments (12-h recovery) with haematoxylin and eosin (H&E) staining to analyse the morphological characteristics of cell death and with immunochemical staining for caspase-3. The preliminary results indicate that there is an increase of caspase-3 immunostaining cells in different regions of the brain, and this effect is diminished by mild hypothermia, particularly in the striatum. We are aware that it is possible to observe the distribution of Bax, Bcl-2 or other proteins involved in cell injury or protection in tissue slices as well as through other measurements suggested by Dr Sakurai. We have used in situ hybridisation and autoradiograms to show that hypoxia induces expression of the 72-kDa heat-shock protein (hsp72) mRNA in different regions of the newborn piglets’ brain and that this was significantly diminished, particularly in striatum, by the depletion of dopamine prior to hypoxia [3]. In another model of hypoxia — repetitive apnoea — we have shown that striatum of apnoeic piglets has a larger number of fluoro-Jade-positive neurons than that of shamoperated animals [4]. Such studies can identify the type of cells affected and the regional specificity of the injury, but at the expense of quantification.

Fatal rupture of splenic artery mycotic aneurysm after mitral valve replacement for infective endocarditis