Mechanism of the Pressor Response to Increased Intacranial Pressure

Abstract

The pressor response to increased intracranial pressure has previously been attributed to an anemia, anoxia or asphyxia of the brain resulting from the increased resistance to inflow of blood into the cranium. The expts. suggest that the pressor response depends on other mechanisms. Thus, severe anoxia induced by breathing 100% N2 or asphyxia following tracheal occlusion produce only a limited increase in blood pressure. During the pressor response to asphyxia, an increase in intracranial pressure produces a new and much greater rise in blood pressure. In the chick the blood pressure response is almost equal to the increase in intracranial pressure. The rate of blood pressure rise is a function of the degree of the intracranial pressure stimulus. Momentary intracranial compression produces an increase in blood pressure often equivalent to the stimulus. The production of the negative intracranial pressure usually results in a fall in blood pressure. These data can be explained by assuming the presence of an intracranial baroceptor similar to that of the carotid sinus. By virtue of its position, it would act as a differential manometer registering the difference between the intravascular and the intracranial pressures. When this difference decreases, vasoconstriction ensues. When the difference is increased, as occurs with decreased intracranial pressure, the vasomotor center responds with vasodilation and a fall in blood pressure.