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(Continued from page 49)
reduces cytotoxic edema. The change that occurs in the cell or interstitially occurs in the CSF approximately 20 minutes later. This change in chemical composition is dependent upon the functional astrocytic uptake as well as the sodium potassium ATPase pump, sodium potassium chloride co-transporter. As the chemical composition increases in concentration, thereby increasing CSF osmolarity, there is increase in CSF protection in order to limit the neuro-toxic effect as does occur on the cellular level. The chloride bicarb exchanger (AE2 isoform) is involved or responsible for the secretion of CSF. The chloride bicarb exchanger is activated with CSF acidosis, or increased CSF potassium. The resultant edema (vasogenic) can be decreased with CSF drainage. Only lowering the CSF pressure does not decrease the edema. During ischemia there are multiple small areas of vasogenic and cytotoxic edema, which coalesce to cause permanent infarct if cerebral blood flow is not reestablished. Therefore, we can prevent infarction if we can reestablish cerebral blood flow and, therefore, we know that edema is readily reversible with improved cerebral blood flow. In addition to increased cerebral blood flow, which occurs with Mannitol and hyperosmolar saline, edema can be reduced by using THAM. This reduces the lactate, the acidosis, the edema and ischemia. This has been shown to be beneficial in humans when given at ten minutes, one hour, or as late as five hours after injury. CT, MR and CSF taurine can readily measure edema. Taurine from two to 20 picomoles per microliter corresponds to the amount of edema. MRI with new diffusion weighted imaging can differentiate between cytotoxic, vasogenic edema as well as areas that have had completed infarctions.
Glutamate neuro-toxicity continues to be investigated as the cause of the majority of the problems associated with brain injury. It is glutamate's relationship with the other neural chemicals and transporters that affect the outcome. The neuro-toxic concentrations of glutamate are now believed to be from the disruption of the cellular membrane integrity and not from synaptic pools. When glutamate is released intracellular it activates the sodium potassium chloride co-transporter, sodium potassium ATPase carrier, and the sodium dependent electronic glutamate carrier. Glutamate increases cell metabolism by increasing glucose metabolism. In turn, more ATP is made to provide energy for the sodium potassium ion pumps. Under anaerobic conditions the TCA cycle produces lactate instead, which cannot be used under anaerobic conditions and it accumulates. Post-synaptically the astrocytes under normal conditions increase glutamate, sodium potassium ATPase dependent uptake in order to prevent ischemia, which would occur from prolonged stimulation. The energy dependent sodium pump (sodium potassium ATPase) generates an inwardly directed electrical chemical sodium gradient that is utilized by the glial-high affinity glutamate transporter to drive the uptake of glutamate. Thus the capacity of astrocytes to maintain the energy dependent sodium (Continued on page 51)
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