Effect of graded anesthesia on laryngeal-induced central apnea

To examine the interaction between laryngeal reflex-induced central apnea and anesthesia, we stimulated the superior laryngeal nerves (SLNs) bilaterally in chronically instrumented piglets (N = 18, age 5-17 days) in the presence of various anesthetic dosages. The SLNs were placed in cuff electrodes and wires were exteriorized in the neck for stimulation. A cannula placed in the aorta was used for blood pressure recording and arterial blood sampling. During each experiment, 1-2 days following surgery, ventilation was recorded using whole body plethysmography, and EEG and ECG were recorded using acutely placed subcutaneous electrodes. Following baseline recordings and before administration of anesthesia, the SLNs were electrically stimulated for 15 min. Following recovery from stimulation, pentobarbital (5-15 mg/kg) was infused and the SLN was stimulated with the same variables for 5 min. Before anesthesia, SLN stimulation caused respiratory frequency (Rf) to fall from 44 +/- 5 (mean +/- SEM) to 16 +/- 2 breaths/min; under anesthesia Rf fell from 33 +/- 7 to 9 +/- 1 (pentobarbital dose a = 16 mg/kg) or from 36 +/- 4 to 3 +/- 1 breaths/min (pentobarbital dose b = 28 mg/kg). PaO2 decreased from 110 +/- 4 to 74 +/- 4 mmHg during stimulation before anesthesia and fell from 100 +/- 6 to 40 +/- 4 with dose a or from 98 +/- 10 to 19 +/- 4 mmHg with dose b under pentobarbital anesthesia. Similarly, choloralose/urethane and ketamine anesthesia enhanced SLN-induced respiratory depression. These results suggest that anesthesia impairs the mechanism responsible for initiating breathing during laryngeal reflex activation.