Is There No Way for the Treatment of Ischemic Brain Edema?
The first event which appears after cerebral ischemia is glial swelling, a feature of cytotoxic edema. At the time of later development of vasogenic edema, any treatment would be of no benefit in the presence of completely infarcted tissue. Thus, effort should be focused on how to manage early cytotoxic edema; otherwise, neurons would die. We therefore sought mechanisms, first at the brain capillaries which display BBB function, and second of the glial membranes which affect the milieu in and around neurons. The currently growing idea is that BBB, i.e., the capillary endothelium retains its morphology and function in cerebral ischemia. In particular, the entry of Na+ in exchange with K+ via Na+, K+-ATPase present at the antiluminal site of endothelium is of great importance in maintaining the extracellular environments for ions and contributing to cell volume regulation. On the other hand, at glial membranes ion antiport mechanisms operate once tissue acidosis has developed. Those ion channels are currently assumed to be Na+/H+ and Cl−/HCO3−to remove H+ from inside the cell, allowing influx of NaCl and H2O. In the present investigations, we sought to elucidate if those mechanisms would be operating at the prenecrotic stage after ischemia, and if some pharmacological manipulations would be possible to relieve not only edema but also neuronal damage.
KeywordsCerebral Ischemia Vasogenic Edema Ethacrynic Acid Cytotoxic Edema Tissue Acidosis
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