STUDIES ON INCREASED INTRACRANIAL PRESSURE AND ITS EFFECTS DURING ANOXIA AND HYPOGLYCEMIA

Abstract

The rise of blood pressure resulting from a rise in the intracranial pressure is a function of the blood pressure-intracranial pressure difference and does not depend upon the absolute intracranial pressure. These observations and the fact that increased intracranial pressure raises the blood pressure in dogs deprived of their buffer nerves in which inhalation of N causes a fall in blood pressure indicate that the effects of intracranial pressure are due to asphyxia of the medulla rather than to anoxia. The inhalation of 7 to 8% O2 potentiates the blood pressure response to raised intracranial pressure in the anesthetized dog. The effect increases with increased duration of the period of anoxia. This potentiation persists in the absence of the buffer nerves. Hypoglycemia also potentiates the blood pressure response to raised intracranial pressure in the anesthetized dog. The effect increases progressively with falling blood sugar. It likewise persists in the absence of the buffer nerves.