Changes in intracranial pressure and arterial blood pressure following electric stimulation to restricted regions in the cat brainstem.

Abstract

The brainstem of anesthetized cats was electrically stimulated to examine the changes in the Intracranial pressure (ICP). There were pressor and depressor sites, which preferentially produced an immediate increase and decrease in ICP in association with the arterial pressor and depressor responses, respectively. A preferential increase in ICP was also observed by stimulation of some depressor sites. The stimulus-induced ICP responses were usually different from the secondary ICP changes due to nonneurogenic alteration of arterial blood pressure (BP) as evoked by arterial bleeding and infusion of saline solution; the stimulus-induced increase in ICP was greatly enhanced when the stimulation to the pressor sites was applied at lowered BP levels and at moderately elevated ICP levels. In addition, when a gradual elevation in ICP was spontaneously observed with the lowering of the BP level, the pressor site-induced increase in ICP exceeded 70-100 mmHg at the peak plateau-like waves, regardless of the magnitude of accompanying arterial pressor response. We propose that the stimulus-induced ICP responses cannot be explained merely by the metabolic changes, the decreased intracranial compliance, and the secondary transmural action on the intracranial space of the arterial pressor and depressor responses. A neurogenic mechanism that directly affects Intracranial blood diameter may be involved in the ICP responses, especially those observed ,at a lower BP level, in addition to extracranic action of sympathetic and parasympathetic nerve activities.

Responses of intracranial pressure (ICP) produced by stimulating the pressor area in the brainstem at various levels of blood pressure and ICP in cats

“…This explanation by the modulated neural activity was supported by the evidence that a moderate elevation of ICP (within about 60 mmHg) produced an alteration in the activity of the cardiovascular sympathetic and parasympathetic nerves (3, 7 , 21) and the findings that the changed B P level and increased ICP level altered the brainstem activity to buffer the blood pressure responses and modified reflex activity to regulate the cardiovascular responses via baroreceptor activation (7, 19). In addition, a low intensity stimulation to brainstem pressor sites sometimes evoked a clear increase in ICP without producing a change in BP (13). The neural control mechanism of intracranial blood vessels on the basis of our findings should be interpreted with caution, especially in relation to possible neural pathways.…”

“…It is of interest, however, that ICP response was increased, even when the pressor response was markedly depressed by a ganglion blocker, which suppresses peripheral sympathetic nerve activity. In addition, a low intensity stimulation to brainstem pressor sites sometimes evoked a clear increase in ICP without producing a change in BP (13).…”

“…Thus, the relationship between an increase in ICP due to dilation of intracranial vessels and changes in BP appears to be related to the brainstem activity in the control of cerebral and systemic circulatory events, whether the increase is induced physiologically or by other means such as electric stimulation (13). In this study, we examined the relation between the increases in ICP and BP evoked by activation of the brainstem pressor sites at different levels of BP and ICP.…”