Neural Organization of Esophageal Peristalsis: Role of Vagus Nerve

Abstract

The purpose of this investigation was 2-fold: first, to determine the velocity of peristalsis in the smooth muscle area of opossum esophagus before and after administration of atropine; second, to evaluate the role of the vagus nerves in the control of the propagative nature of esophageal peristalsis. Intraluminal pressures were measured through a pressure transducer recorder system attached to continuously perfused catheters. The velocity of peristalsis in the lower third of the esophagus progressively decreased from 3.25 plus or minus 0.20 (SE) cm per sec at the 70 to 80% level to 2.17 plus or minus 0.14 (SE) at the 80 to 90%level to 1.83 plus or minus 0.10 (SE) at the 90 to 100% level. After administration of intraperitoneal atropine (100 mug per kg), the velocities were 3.1 plus or minus 0.26 (SE) cm per sec, 2.38 plus or minus 0.22 (SE), and 1.74 plus or minus 0.10 (SE), respectively, at the 70 to 80%, 80 to 90%, and 90 to 100% levels. The changes were not statistically significant. Electrical stimulation of the distal cut end of the vagus nerve induced peristaltic contractions. The velocities of peristalsis after electrical stimulation of the vagus nerve were 3.24 plus or minus 0.72 (SE) cm per sec, 2.81 plus or minus 0.64 (SE), and 1.84 plus or minus 0.34 (SE), respectively, at the 70 to 80%, 80 to 90%, and 90 to 100% levels. Results of this study indicate that the velocity of peristalsis in the smooth muscle area of the opossum esophagus has a caudally decreasing gradient. Bilateral cervical vagotomy and stimulation of the distal cut end initiates peristaltic contraction indicating that the propagative nature of peristalsis in the smooth musurrent, does not alter mucosal cyclic AMP. Dibutyryl cyclic AMP decreased net sodium absorption and increased short circuit current; findings which were qualitatively identical to those produced by taurochenodeoxycholic acid. These studies support the proposal that bile salts stimulate colonic electrolyte secretion by increasing mucosal cyclic AMP.