We thank Drs. Toumpoulis and Anagnostopoulos for their valuable comments regarding our article.1As they indicated, hypotension during the reperfusion period after ischemic preconditioning may be an important factor for its neuroprotective efficacy. In our study, transient hypotension was in fact observed in animals with ischemic preconditioning, but this returned spontaneously to the baseline within a few minutes after the reperfusion. Consequently, there were no statistical differences in blood pressure among the groups at baseline before lethal ischemia. We cannot rule out the possibility that this transient hypotension might have affected the neuroprotective efficacy by ischemic preconditioning. However, compared with the method (20 min of brief ischemia) of Toumpoulis et al. ,2we used only 5 min of ischemia as preconditioning. The degree of hypotension observed in our study might be less than that in their study.
As one possible mechanism by which ischemic preconditioning can induce tolerance to subsequent ischemia, it has been suggested that an antiinflammatory process may be involved.3However, the data are still limited, especially in a situation of rapid ischemic preconditioning for the spinal cord. Unfortunately, so far, we have not performed further histologic assessments regarding the grade of inflammation. Further study is required.
* Nara Medical University, Nara, Japan. email@example.com