Characterization and mechanisms of the pharyngoesophageal inhibitory reflex.

The objectives of this study were to identify and to characterize the pharyngoesophageal inhibitory reflex (PEIR) in an animal model. Thirty-one cats (2.4-5.0 kg) were anesthetized using alpha-chloralose (45 mg/kg ip), and esophageal peristalsis was recorded manometrically. Secondary peristalsis was activated by rapid air injection (8-20 ml) at midesophagus or slow infusion of water through the manometric catheters. Neither stimulus activated primary peristalsis. The PEIR was activated by rapid water injection or focal mechanical stimulation of the pharynx. Rapid air injection activated secondary peristalsis in 92% of the trials, and slow water infusion activated 1 secondary peristalsis every 3.2 min. Pharyngeal stimulation by 0.3, 0.5, 0.8, or 1.0 ml of water inhibited or blocked ongoing secondary peristalsis in 67, 82, 97, or 93% of trials, respectively. Mechanical stimulation of the posterior wall of the pharynx with 11-20 g pressure attenuated secondary peristalsis in 96% of the trials or blocked secondary peristalsis in 41% of the trials. Centripetal electrical stimulation at 30 Hz, 0.2 ms, 2 V for 4 s of the superior laryngeal (SLN) or glossopharyngeal (GPN) nerves blocked or inhibited secondary peristalsis in 100% of the trials. Bilateral transection of the GPN (n = 8), but not the SLN (n = 6), blocked the PEIR. Anesthetization of the pharyngeal mucosa using lidocaine (2%) blocked the PEIR (n = 3). We concluded that 1) the PEIR exists in the cat, 2) mechanical stimulation of the pharynx more strongly activates the PEIR than water, 3) activation of either SLN or GPN afferents attenuates ongoing secondary peristalsis, 4) the receptors mediating the PEIR are located in the pharyngeal mucosa, and 5) both SLN and GPN contribute to the PEIR, but the GPN is the major afferent limb of this reflex.