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Dysphagia Institute and Department of Medicine, Medical College of Wisconsin, Milwaukee, Wisconsin 53226
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
-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.
pharynx; esophagus; glossopharyngeal nerve; superior laryngeal nerve; esophageal peristalsis; secondary peristalsis
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