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tumor or other instances when vasogenic edema can occur and would lead to further complications. It has been well known since the 1960s that dexamethasone stabilizes the blood brain barrier and even decreases the permeability to other lipid soluble chemicals. It may also be stabilized by copper, zinc, superoxide dismutase and serotonin antibodies. The specific serotonin type has not been demonstrated. In contrast 5-hydroxytryptamine 1A, a type of serotonin, itself decreases edema why also, and unfortunately, decreasing mean arterial pressure. A promising medication that has been used multiple times in humans is progesterone. Progesterone at 4 mg./kg. better reduces human edema than methylprednisolone.
There are three types of edema; vasogenic, cytotoxic, and hydrocephalic or interstitial. In cytotoxic or cellular edema, the mechanism involved is the intracellular metabolic machinery and/or metabolic substrates. In vasogenic edema it is the increased capillary permeability and in the interstitial form it is the generation of transependymal pressure gradients forcing CSF from the ventricle to the extra-cellular space. Cytotoxic edema is swelling in the glial cells, which is an attempt to buffer the neuro-toxins, lactate, potassium ion, hydrogen ion, glutamate, oxygen free radicals and others, to prevent injury. Cytotoxic edema is the major contributor to traumatic brain injury; it is not vascular engorgement and vasogenic edema. Vasogenic edema occurs medially and cytotoxic edema starts to occur 30 minutes to one hour after injury and can peak in one to two weeks. The glial cells swell because the glycogen granules increase in number, thereby drawing water in, the glycogen granules increases in number to utilize more energy for the TCA cycle in order to actively transport mean metabolites out of the cell. Cytotoxic edema is an extremely complex phenomenon and is stimulated or attenuated by the cellular transport systems. These systems are sodium potassium ATPase, sodium potassium chloride co-transporter, calcium activated potassium channels, sodium hydrogen antiporter, and chloride bicarb exchanger. All save the last are stimulated by endothelin. In cytotoxic edema there is initially an influx of extracellular calcium or independently free fatty acids which possibly stimulate sodium phosphorylation of protein kinase C, leading to an increase in intracellular hydrogen and edema. It may also be that serotonin, prostaglandins and opioids stimulate cyclic AMP dependent ion transport causing an increase in intracellular hydrogen ions and once again causing edema. Hydrogen ions (acidosis) are what appear to be most commonly seen as the cause of cytotoxic edema. The hydrogen ions are either directly brought into the cell or are a result of lactic acidosis. There are drugs that work at both sites. Alpha-trinositol inhibits the sodium hydrogen ion antiporter, preventing the accumulation of intracellular hydrogen ions, and edema. Also inhibiting the sodium hydrogen ion antiporter as well as the sodium calcium exchange is the potassium sparing diuretic, amiloride (5 mg. q. 12 hours) that prevents increased intracranial pressure and (Continued on page 50)
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