INITIATION OF ESOPHAGEAL SECONDARY PERISTALSIS BY SLOW FLUID INFUSIONIN THE OPOSSUM - EFFECT OF HYDROCHLORIC-ACID

We investigated the mechanisms of slow fluid infusion-induced secondar y peristalsis and the effects of hydrochloric acid on this response. I n 13 chronically esophagostomized opossum, acidic and neutral barium s ulfate were infused into the distal esophagus at a rate of 1.1 ml/min, while recording the esophageal dimension by videofluoroscopy and esop hageal intraluminal pressure concurrently. The effects of atropine, te trodotoxin, capsaicin, and bilateral cervical vagotomy on the response to slow fluid infusion were examined. Acidic barium initiated seconda ry peristalsis more frequently and at shorter latency with less increa se of preperistaltic intraesophageal pressure than neutral barium (P < 0.05). Atropine abolished secondary peristalsis initiated by neutral barium. For acidic barium, atropine decreased the incidence of seconda ry peristalsis, increased the latency for initiation of secondary peri stalsis, and initiated secondary peristalsis more distally (P < 0.05). Tetrodotoxin or vagotomy and capsaicin abolished activation of second ary peristalsis. We concluded that secondary peristalsis can be stimul ated in response to slow distension by minute amounts of fluid. This p eristalsis is atropine and capsaicin sensitive and vagally mediated. T he presence of acid significantly lowers the threshold for stimulation of secondary peristalsis induced by slow fluid distension. This effec t seems to be atropine resistant.