Radial distribution of esophageal peristaltic pressure in normal subjects and patients with esophageal diverticulum.

This study was designed to determine the radial profile of peristaltic pressure waves in the esophageal body of normal subjects and patients with isophageal diverticulum. We used a manometric assembly featuring four radial side hole recording orifices oriented at equidistant 90 degree angles. Each recording catheter was infused with water at a rate (6.1 ml per min) which provided high fidelity pressure recording. In normal subjects, the radially recorded peristaltic pressure complexes were similar in peak amplitude and wave form. The range of pressure differences between the four radial recordings averaged 9.0 +/- 4 SD mm Hg A range is less than or greater to 25 mm Hg occurring in 99% of observations. These variations in pressure amplitude showed no consistant spacial orientation. In 5 of the 6 patients with esophageal diverticulum, the range of radial peristaltic pressure differences exceeded 25 mm Hg in the region of the diverticulum, the lowest pressure occurring at the recording orifice facing the diverticulum mouth. In occasional peristaltic sequences abnormal wave forms featuring abrupt onsets or offsets were observed. These bizarre wave forms were probably caused by oralaboral diverticulum movement relative to the recording sensor during peristalsis. Two patients had abnormally high peristaltic pressure amplitudes, greater than 250 mm Hg. This latter finding introduces the possibility that hypertensive peristaltic contractions may contribute to diverticulum production in some patients.

Lower esophageal sphincter responses to enteric hormones in two patients with Zollinger-Ellison syndrome.

The effect of exogenous glucagon and secretin on resting lower esophageal sphincter (LES) tone during endogenous hypergastrinemia was studied in 2 patients with proven Zollinger-Ellison Syndrome (ZES). Intravenous glucagon and in one patient secretin, in dosages which decrease LES pressure in normals during LES stimulation by exogenous gastrin, caused a decrease in resting LES pressure in the ZES patients. This drop in LES tone occurred both during concomitant serum gastrin rise caused by secretin and serum gastrin decline caused by glucagon. This finding suggests that the action of secretin on LES pressure may be independent on endogenous gastrin, while the glucagon effect on LES tone may be mediated through gastrin.

Effect of glucagon on esophageal motor function.

This study evaluates the effect of exogenous glucagon on esophageal motor function in man. Manometric studies were performed using an infused catheter system. Resting lower esophageal sphincter (LES) pressure was monitored before and after intravenous pulse doses of glucagon (1 to 100 mug). The effect of glucagon (0 mug ) on esophageal peristalsis was also studied. Multiple blood samples were taken for determination of glucagon, insulin, and glucose concentration. Glucagon effect on LES pressure was also evaluated after LES stimulation by continuous intravenous infusion and pentagastrin (0.04 mug per kg per min). Glucagon caused a transient significant decrease of LES pressure only at pulse doses (20 and 100 mug) which caused nonphysiological elevation of plasma glucagon levels. The temporal profile of decreased LES pressure correlated closely with maximal blood glucagon levels. Glucagon caused no demonstrable change in esophageal peristalsis. During LES stimulation by pentagastrin, glucagon caused significant transient decreases of LES pressure at doses as low as 1 mug per kg. We conclude that glucagon at sufficient dosage has an inhibitory effect on LES pressure. This inhibitory effect is not mediated through changes in serum insulin or glucose and appears to be pharmacological.