Key result
Acute intracranial compression triggers immediate hypertension and expands circulating blood volume by ~10%.
A sudden rise in intracranial pressure initiates a three-fold cardiovascular response in the dog. Within one second after the onset of compression, the blood pressure rises sharply, presumably as a result of a direct neurogenic stimulus to the arterioles; the pressure then levels off in a few seconds. A second pressor effect is apparently due to the secretion into the blood stream of graded amounts of nor-epinephrine-like materials at the onset of compression; this rise is delayed about 12 seconds, a period perhaps associated with its circulation to the arterioles. In some experiments, a heart rate increase occurs at this time. It is shown by a special technique that the circulating blood volume increases about 10 per cent during this period. With the offset of compression all these effects disappear in the same order. The potential role of these mechanisms in the blood pressure regulating complex is discussed.
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Rodbard et al. (1955) studied Cardiovascular response to intracranial compression. Intracranial compression was evaluated on Cardiovascular response (blood pressure, heart rate, circulating blood volume). Sudden intracranial compression in dogs induced a rapid blood pressure rise, a secondary norepinephrine-mediated pressor effect, and a 10% increase in circulating blood volume.
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