Lidocaine in the Rat Rostral Hypothalamus: Effect on Arterial Carbon Dioxide 1

Abstract

Abstract

Lidocaine hydrochloride causes an increase in respiratory frequency (f) when infused into the rostral hypothalamus of the rat. The purpose of our study was to determine whether this increased f was primarily due to: (i) a direct increase in neural respiratory drive; (ii) a change in metabolism, mediated by the hypothalamus, causing increased carbon dioxide production and secondary hyperpnea; or (iii) a combination of these phenomena. Arterial carbon dioxide tension (P _aCO₂),f, and tidal volume (V _t) were measured in awake, unrestrained, tranquilized rats before and after the infusion of either lidocaine or hypertonic saline into the rostral hypothalamus. At peak increase in f, approximately 2 min after lidocaine infusion, f had increased 26.5 breaths/min (28.3%), P _aCO₂ had decreased 3.5 mm Hg (10.3%), and V _t was unchanged. There was no change inf, V _t, or P _aCO₂ 2 min after saline infusion. Since an increase in carbon dioxide production typically causes increased ventilation with a stable P _aCO₂, the increasedf and hypocapnia seen following infusion of the local anesthetic lidocaine are best explained by a depression of inhibitory neural discharge from the rostral hypothalamus resulting in increased discharge from the lower brainstem respiratory control centers.