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Almost all of the oxygen consumed by the brain is utilized for the oxidation of carbohydrate. Sufficient energy is released from this process so that the normal level of oxygen utilization is adequate to replace the 12 mmol or so of A TP which the whole brain uses per minute. However, since the normal brain reserve of A TP and creatine phosphate (CrP) totals only about 8 rnmol, less than a minute's reserve of high energy phosphate bonds is actually available if production were to suddenly stop. In the absence of oxygen, the anerobic glycolysis of glucose and glycogen could supply only another 15 mmol of A TP, as these two energy substrates are stored in such low quantities in brain tissue.

A continuous uninterrupted supply of oxygen to the brain is essential in order to maintain its metabolic functions and to prevent tissue damage. The ox­ygen-independent glycolytic pathway (anerobic glycolysis) is insufficient, even at maximum operating levels, to supply the heavy demands of the brain. Thus a loss of consciousness occurs when brain tissue P0₂ levels fall to 15 to 20 mmHg. This level is reached in less than 10 s when cerebral blood flow is com­pletely stopped

Low tissue oxygen levels in the brain (hypoxidosis) can be caused by de­creased blood flow (ischemia) or with adequate blood flow accompanied by low levels of blood oxygen (hypoxemia). It is important to recognize that decreased P0₂ caused by ischemia is accompanied by decreased brain glucose and in­creased brain CO₂ while hypoxemia with normal blood flow is not accompanied by changes in brain glucose or CO₂, with complete cessation of CBF, irreversible damage occurs to brain tissue within a few minutes and the histological ef­fects observed are remarkably similar whether caused by ischemia, hypoxemia, or hypoglycemia.

Experimental studies on rats and mice in which arterial P0₂ is progres­sively reduced have illustrated some aspects of hypoxemia which are likely to be similar in humans. A drop in arterial P0₂ to 50 mmHg (normal, 96 mmHg) produces no change in CBF, O₂ utilization by the brain, or lactic acid produc­tion. However, as P0₂ levels drop to 30 mmHg, a 50 percent increase in CBF is observed along with the onset of coma, decreased oxygen utilization, and in­creased lactic acid production. When the P0₂ drops further to 15 mmHg, 50 percent of the animals die because of cardiac failure. The remainder show a tremendous increase in lactic acid production, but, surprisingly, levels of ATP, ADP, and AMP remain normal. If cerebral perfusion is artificially maintained while the arterial P0₂ is decreased further, ATP, ADP, and AMP levels still remain normal. The implication is that the coma observed at low oxygen levels may not be due to a decrease in ATP but instead to some still unexplained mechanism. It appears likely that cardiac complications caused by hypoxemia and the subsequent effect on cerebral blood flow may actually be a primary cause of the irreversible pathologic damage to the brain.

Hypoxia, such as that brought on by high altitudes, brings on a number of symptoms, including drowsiness, apathy, and decreases in judgment. Unless oxygen is administered within half a minute or so, coma, convulsions, and depression of the EEG occur.