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Anesthesia Prolongs the Apneic Duration Elicited by Intracarotid Injection of Capsaicin in Decerebrate Rats
Rurong Wang, M.D., Fadi Xu, M.D.
Pathophysiology Program, Lovelace Respiratory Research Institute, Albuquerque, New Mexico, United States.
Introduction: Activation of bronchopulmonary C-fibers (PCFs) via right atrial injection of capsaicin (CAP) induced an apnea and hypotension in both anesthetized and un-anesthetized animals, which rely on the brainstem respiratory network. Recently, we reported that intracarotid injection of CAP produced a longer apnea associated with a pressor response, independent of PCF inputs in anesthetized rats. This finding suggests that stimulation of carotid sinus C-fibers and/or neurons in the central nervous system is capable of substantially inhibiting inspiration. In the present study, our goal was to define whether the cardiorespiratory responses we observed exist after removal of the cerebrum, and, if so, whether anesthetic status affects the response.

Methods: Experiments were conducted in anesthetized, tracheotomized, and spontaneously breathing rats (n = 8). Pentobarbitone (40-50 mg/kg, IP) was used for initial anesthesia. According to a short effective duration of pentobarbitone (approximately 90 min in adult male rats; Laboratory Animals, Field, et al., 1993), we defined discontinuing anesthetic for 3-4 hr as un-anesthetized state. Decerebration was performed immediately after adding supplemental anesthetic (10-12 mg/kg, IV). In four rats, intracarotid injections of vehicle and a threshold dose of CAP (4ng, 16ng, 64ng) to produce an apnea were administered 20 min and 3-4 hr after decerebration. In the others, supplemental anesthetic was added 3-4 hr after decerebration, and vehicle and CAP injections were performed 3 min before and immediately after this supplemental anesthetic. A paired t-test was used to compare the baseline cardiorespiratory values before and after decerebration, while two-way repeated measures ANOVA followed by Fisher's LSD test was utilized for comparing these responses to injections ( Δ% change from control ) between the anesthetized and un-anesthetized rats. A P value < 0.05 was considered as significant.

Results: Removal of the cerebrum significantly increased tidal volume ( from 1.37 ± 0.14 to 2.18 ± 0.23 ml, P < 0.05 ) and minute ventilation ( from 75 ± 6 to 124 ± 16 ml/min, P < 0.05) with no significant effect on cardiovascular activities. Intracarotid injection of CAP significantly increased expiratory duration (TE, i.e., apnea) and mean arterial blood pressure (MABP) with no effect on heart rate (HR) when compared with vehicle injection [Table 1]. Moreover, as compared to adequate anesthesia, this CAP-induced apnea was significantly shortened with little effect on the pressor response 3-4 hr after discontinuing supplemental anesthetic [Table 1].

Conclusion: Our data suggest that the brainstem respiratory network, rather than the cerebrum, is essential for generating the CAP-induced apnea. This brainstem-mediated apneic reflex is strengthened by, but not dependent on, anesthesia.

Anesthesiology 2004; 101: A1547
Table 1: Comparison of the cardiorespiratory values induced by CAP between the anesthetized and un-anesthetized rats
TE (Δ%)MABP (Δ%)HR (Δ%)
Anesthetized1.5 ± 0.9353.1 ± 68.4∗†1.1 ± 0.939.7 ± 8.0∗0.5 ± 0.43.9 ± 2.6
Un-anesthetized1.0 ± 0.3166.6 ± 28.5∗1.4 ± 1.339.3 ± 6.2∗0.7 ± 0.17.3 ± 4.8
means ± SE, N = 12 trials in 8 rats, ∗P < 0.05 compared with vehicle, †P < 0.05 compared between the anesthetized and un-anesthetized rats