The study evaluates the triggering and characteristics of secondary oe
sophageal peristalsis in 25 healthy volunteers. Secondary peristalsis
was stimulated by rapid intraoesophageal injection of boluses of air a
nd water, and by a five second oesophageal distension with a ballon. A
ir and water boluses triggered secondary peristalsis that started in t
he proximal oesophagus regardless of injection site. Response rates we
re volume dependent with 83% of the 20 mi air boluses triggering secon
dary peristalsis compared with 2% for the 2 mi water bolus (p<0.0001).
Response rates for air and water were similar for equal bolus volumes
and were not influenced by the site of injection. In contrast, balloo
n distension usually induced a synchronous contraction above the ballo
on, with secondary peristalsis starting below the balloon after deflat
ion. The peristaltic response rate to balloon distension was also volu
me dependent and the middle balloon was more effective in triggering s
econdary peristalsis than either the upper or lower balloons (p<0.001)
. Secondary peristaltic amplitude was less than that of primary perist
alsis (p<0.001). Secondary peristaltic velocity with a water bolus was
slower (p=0.001) than that of primary peristalsis. Intravenous atropi
ne significantly reduced secondary peristaltic responses to all stimul
i. There was also a significant reduction in pressure wave amplitude f
or air stimulated secondary peristalsis while those for the water resp
onses were similar. Secondary peristaltic velocity with air and water
boluses was not changed by atropine. The reproducibility of testing se
condary peristalsis was examined six volunteers and did not show any s
ignificant differences on separate test days in response rate and peri
staltic amplitude or velocity. It is concluded that in normal subjects
, secondary peristalsis can be more reliably triggered by intraoesopha
geal air or water infusion than balloon distension. Secondary peristal
tic amplitude and velocity are stimulus but not site or volume depende
nt and propagation is partially mediated by cholinergic nerves.