Tonus sympathique et activité électrique corticale

Abstract

Simultaneous recording of the electrical activity of the cortex and of the arterial blood pressure in animals (cats and dogs) under Flaxédil demonstrates the following: 1. 1. In an animal which has no external sensory stimulation, there is a spontaneous fluctuation in the electrical activity of the cortex and also in the level of sympathetic tone. These variations both in the electrical activity of the cortex and in sympathetic tone are always synchronous and parallel; activation of the cortex corresponding with an increase (even a small one) in the blood pressure. 2. 2. Nociceptive stimuli (e.g. electrical stimulation of the sciatic nerve) produce a marked cortical activation and an increase in sympathetic tone (vasomotor effects and adrenaline secretion, etc.). Analysis of the effects of such stimuli under different experimental conditions, shows that: 2.1. ( a) the duration of the cortical activation after the nociceptive stimulus is directly related to the intensity of the sympathetic response; 2.2. ( b) while pre-bulbar section completely eliminates the possibility of putting into action the reticular activating system of Moruzzi and Magoun by means of nociceptive stimulation, peripheral sympathetic discharge is still preserved. However, there is still an intense cortical activation corresponding with increase in sympathetic tone, but this activation appears later, i.e. during the ⪡adrenaline phase⪢ of the hypertension produced by sciatic stimulation; 2.3. ( c) stimulation of the peripheral end of the splanchnic nerve or injection of adrenaline, either in the normal animal or in the animal after pre-bulbar section, produces an intense activation of all cortical areas, an activation which develops in parallel with the increase in peripheral sympathetic tone; 2.4. ( d) intercollicular section of the brain stem, passing to the ventral surface just rostral to the pons (section A, fig. 18) completely suppresses the cortical activation in response to a peripheral sympathetic discharge. After a section slightly more caudal (section B, fig. 18) this cortical activation persists. Cortical activation corresponding with a peripheral sympathetic discharge is therefore not due to a direct action of adrenaline or to the increase of blood pressure (both of which factors are of course interrelated) on the cortex, but to an action on pontomesencephalic formations; 2.5. ( e) cortical activation in response to an nociceptive stimulus therefore occurs by means of two mechanisms which, in general, overlap each other: (i) an immediate nervous activation which operates by means of a mechanisms which is now well known, i.e., through the ascending reticular activating system, and, (ii) by means of a subsequent “humoral” activation which also works not directly on the cortex but through pontomesencephalic formations; 2.6. ( f) the “humoral” activation allows an adjustment of cortical activity to the peripheral sympathetic activity existing at the moment. The fact that the increase in sympathetic tone (adrenaline, slight hypertension) is able to produce an electrical picture of cortical activation which is indistinguishable from that produced by an exteroceptive stimulus, suggests that the level of peripheral sympathetic tone is just as important a factor in maintaining the waking state as the continuous inflow to the brain of proprioceptive and exteroceptive stimuli. 2.7. 3. All these effects on cortical activity of a peripheral sympathetic discharge are suppressed by very small doses of anaesthetics. 2.8. 4. Distention of the carotid sinus (within physiological limits) produces a progressive reduction in cortical activity and the appearance of slow waves. This effect is still seen after high spinal section combined with bilateral vagotomy, a procedure which suppresses the hypotensive response to carotid sinus distention, and which suppresses in the same time direct effects from the carotid sinus on the vasomotor control of the cerebral circulation. The reduction in cortical activity in response to carotid sinus distension is therefore independent of variations in the blood pressure and is mediated by purely nervous mechanisms. This appears to be the first example of an afferent inflow which “damps” rather than activates the cortex. 2.9. 5. The experimental facts described in this paper have been integrated in a provisional schema of the regulatory mechanisms responsible for the continuous adjustment and interrelations of cortical activity and peripheral sympathetic tone.