We have demonstrated respiratory chemosensitivity to changes in (H+) and Pco2 of the cerebrospinal fluid (CSF) in the subarachnoid space on the ventrolateral surface of the medulla. Respiratory stimulation was elicited from this region by increased Pco2 and (H+), nicotine, and acetylcholine; and respiratory depression by procaine, NaCN, lobeline, cold CSF, decreased Pco2 and (H+). CSF made acid by high (Cl-) at constant Pco2 moved the entire CO2 response curve to the left and was a more effective stimulus than normal CSF made acid by equilibration at high Pco2, presumably because of rapid diffusion loss of CO2 from the perfusing CSF into the underlying tissue and blood. Steady rapid perfusion of this area with a mock CSF of normal (H+) and Pco2 had no effect on respiration but depressed the respiratory response to inhaled CO2 by 40%. When placed in the fourth ventricle, procaine and high (H+) and Pco2 did not affect respiration, but nicotine and acetylcholine depressed it. This suggests that part of the medullary respiratory response to inhaled CO2 originates in an (H+)-sensitive surface exposed to CSF on the ventrolateral medulla.
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Mitchell et al. (1963) studied this question.