To save content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about saving content to .
To save content items to your Kindle, first ensure firstname.lastname@example.org
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about saving to your Kindle.
Note you can select to save to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be saved to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
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.
The blood–brain barrier (BBB), formed by the cerebral endothelial cells and their connecting tight junctions, has a very low permeability to ions unless specific transporters are present. The endothelial movement of ions, via either ion transporters or ion channels, has a number of important functions. It is involved in the regulation of several key ion concentrations in the brain (e.g. K+, Ca2+, H+), the uptake and extrusion of trace metals, fluid secretion and, by linkage to the endothelial sodium gradient, nutrient transport. Ion transport is also important in regulating BBB function. For example, changes in endothelial cell [Ca2+] and volume modulate BBB integrity (Rapoport et al., 1980; Olesen and Crone, 1986).
Understanding ion transport at the BBB may aid in the treatment of a number of disease states, particularly those such as stroke where edema formation results from a net accumulation of ions and thus water in the brain (Betz et al., 1994). However, despite the importance of BBB ion transport in normal and pathophysiological conditions and its potential for modulating BBB function, our knowledge of ion transport and its regulation is still far from complete. This particularly reflects the limitations of in vivo BBB experimentation and deficiencies in current in vitro preparations. Although such difficulties apply to all studies of the BBB, they are particularly pertinent to ion transport because of the low rate of transport.
Email your librarian or administrator to recommend adding this to your organisation's collection.