Modulation of the centrally-evoked visceral alerting/defence response by changes in CSF pH at the ventral surface of the medulla oblongata and by systemic hypercapnia

In the present study on nine cats, repeated tests were made of the effects of superfusion of the ventral surface of the medulla oblongata with acid or alkaline CSF. Only two animals showed slight hyperventilation, tachycardia, mesenteric vasoconstriction and variable changes in hindlimb vascular conductance when the ventral surface was superfused with acid CSF; alkaline CSF produced opposite effects. These changes are qualitatively similar to, but much smaller than, published results which support the idea that the central chemoreceptor areas for CO₂ are near the surface of the ventral medulla. But, in accord with those who have disputed this idea, the remaining 7 animals showed no response to superfusion with acid or alkaline CSF. Yet, all 9 animals showed marked hyperventilation in response to inhalation of 5% or 8% CO₂. These findings accord with the view that chemosensitive structures on the ventral medulla represent part, but not all of the central chemsensitive mechanism for CO₂. Inhalation of CO₂ also induced bradycardia, mesenteric vasodilatation and either vasodilatation or vasoconstriction in hindlimb, attributable to a predominance of the direct myocardial depressant and local vasodilator effects of CO₂, over the increase in sympathetic activity produced by central hypercapnia. But, despite the different effects of acid CSF and inhaled CO₂ on baselines, they produced comparable effects on the visceral altering/defence response evoked by electrical stimulation in the ventral amygdalo-hypothalamic pathway viz, the magnitude of the characteristic hindlimb dilatation was reduced while that of the mesenteric constriction was increased. This could be explained if an increase in H⁺ ion concentration in the ventral medulla facilitates transmission from the efferent pathway from the defence areas on to the neurones of nucleus paragigantocellularis, PGL, which mediate the visceral altering response. The possibility is also raised that other reported effects of changes in the pCO₂ and pH of CSF at the ventral surface may be explained by an action of H⁺ ions on synaptic transmission in PGL or other neuronal structures in the ventral medulla, rather than by an action on specific chemoreceptors. Irrespective of the precise mechanisms involved, the observed results suggest that a reduction in brain ECF pH produced for eg, by systemic hypercapnia or a change in CSF pH, may by an action in the ventral medulla, accentuate the pressor effect of the visceral alerting response evoked by excitatory inputs to the brainstem defence areas.