Catechol changes in the rat rostral ventrolateral medulla following changes in systemic CO2.

A catechol signal recorded with in vivo voltammetry within the rat rostral ventrolateral medulla (RVLM) was taken as an index of the activity of RVLM adrenergic neurons and related to the level of arterial PCO2, under halothane anesthesia. Reversible increases in catechol signal were observed during reversible increases in arterial partial CO2 pressure (PaCO2) from 20 to 60 mmHg after alteration of tidal volume (n = 5 intact rats, n = 5 after carotid sinus deafferentation). A reversible increase in inspiratory CO2 combined with constant tidal volume led to changes in PaCO2 from 40 mmHg to 50 or 60 or 70 mmHg for 60 min (n = 5 in each group) and to a reversible increase in catechol signal (r = 0.76). These changes were also observed after carotid sinus deafferentation (PaCO2 = 40 to 60 to 40 mmHg, n = 5). Lowering the PaCO2 from 40 to 20 mmHg led to a minor, nonsignificant reduction in catechol signal (n = 5). Changes in arterial pressure were minimal, although they reached statistical significance in some groups of experiments. The level of catechol metabolism in the RVLM 1) is continuously related to the level of arterial CO2, 2) functions close to its resting level under baseline nonstimulated condition with respect to CO2, and 3) is reversibly modified on changes in capnia. Sensitivity of the catechol signal, recorded in the rostral ventrolateral medulla, to CO2 appears primarily to be centrally mediated. Thus adrenergic RVLM neurons may relay inputs from the central respiratory generator to the sympathetic chemoreflex or act as chemosensors for CO2, next to the ventrolateral medulla surface.