Summary
There is increasing evidence that cerebral ischemic injury occurs at a slower pace than previously believed. Although in areas of severe ischemia tissue damage occurs relatively rapidly, in regions of less-severe ischemia, damage develops over the course of many hours or even days. In this chapter, we review data indicating that inducible nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2) are upregulated following focal cerebral ischemia and that the products of their reaction contribute to the delayed progression of ischemic brain damage. Administration of iNOS and COX-2 inhibitors may be a useful therapeutic strategy to selectively target the progression of the brain damage that takes place during the post-ischemic period.
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Iadecola, C., Ross, M.E., Zhang, F., Nogawa, S., Nagayama, M., Nagayama, T. (1999). Delayed Gene Expression and Ischemic Brain Injury. In: Ito, U., Fieschi, C., Orzi, F., Kuroiwa, T., Klatzo, I. (eds) Maturation Phenomenon in Cerebral Ischemia III. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-58602-6_3
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DOI: https://doi.org/10.1007/978-3-642-58602-6_3
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