RAPID CHANGES IN CEREBRAL OXYGEN TENSION INDUCED BY ALTERING THE OXYGENATION AND CIRCULATION OF THE BLOOD

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Abstract
Using a standard polarographic procedure, O2 tension was measured with a platinum electrode encased in a small glass tube surrounded by a larger tube containing saline agar in which the Ag-AgCl positive electrode is buried. With such an electrode and suitably adjusted voltage, it is possible to record the O2 tension of tissue in vivo as a function of the amperage. By this method, studies were carried out on the cortices of cats anesthetized with Dial or immobilized with /? erythro-idine. A decrease in cortical O2 tension invariably followed erythroidinization; this was believed to be due to a decrease in cerebral blood flow secondary to a decrease in systemic blood pressure. When adrenalin or ephedrine were administered, an increase in cerebral O2 tension occurred; this was believed to be due to an increase in cerebral blood flow secondary to a rise in systemic blood pressure. Amyl nitrite caused a fall in O2 tension probably secondary to the fall in systemic blood pressure. Ergotamine tartrate and nicotinic acid had insignificant effects. Inhalation of N produced a precipitous fall in cortical O2 tension to a low level which was considered asphyxial. With the readmission of air, the cerebral O2 tension rose rapidly to a level above that observed before asphyxiation. Breathing O2 raised the cerebral O2 tension.

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