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Chapter 18 - Thrombin and secondary brain damage following intracerebral hemorrhage

Published online by Cambridge University Press:  04 May 2010

J. Ricardo Carhuapoma
Affiliation:
Johns Hopkins Hospital, Baltimore
Stephan A. Mayer
Affiliation:
Columbia University, New York
Daniel F. Hanley
Affiliation:
Johns Hopkins Hospital, Baltimore
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Summary

Thrombin is an essential component of the coagulation cascade and forms immediately in the brain after an intracerebral hemorrhage (ICH). This chapter discusses the evidence concerning the role of thrombin in secondary brain injury following ICH. Thrombin enhances the synthesis and secretion of nerve growth factor in glial cells, modulates neurite outgrowth, and reverses process-bearing stellate astrocytes to epithelial like astrocytes. Thrombin also stimulates astrocyte proliferation and modulates the cytoskeleton of endothelial cells. The effects of thrombin in the brain are modulated by endogenous serine protease inhibitors. Thrombin is responsible for early brain edema development after ICH. Intracerebral injection of thrombin induces brain edema. Modulating thrombin activity in the brain may establish novel therapeutic strategies for ICH. However, because of the dichotomy in the effects of thrombin on brain injury, it is essential to delineate the pathways involved in the deleterious and beneficial effects of thrombin on brain injury.
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Publisher: Cambridge University Press
Print publication year: 2009

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