The complained gastrointestinal symptoms in PSS are probably caused by several complex disturbances like intestinal transit disturbances (ITD), bacterial overgrowth of the small intestine caused malabsorption of bile acids and altered kinetics of intestinal hormones. 25 patients with PSS and eleven healthy controls were tested for the existence of ITD by use of the metal-detector test (MDT). Twelve patients were also tested for a malabsorption of primary bile acids by radioimmunological measurement of clolylglycine serum levels before and after a meal. In addition serum concentrations of gastrin (nine patients) and plasma concentrations of cholecystokinin (CCK) (eight patients) and motilin (eleven patients) were measured by radioimmunoassay pre- and postprandial. Interdigestive gastric emptying was accelerated in patients with PSS (53 +/- 3 min. vs. 73 +/- 7 min.; p<0.01). Small intestinal transit times were similar in both groups (115 +/- 17 min. vs. 121 +/- 13 min.). Colonic transit in patients with PSS was significant prolonged (63 +/- 6 h vs. 39 +/- 5 h; p<0.05). There were no significant differences between the two groups concerning the pre- and postprandial levels of cholylglycin. Basic and postprandial levels of gastrin, CCK and motilin were higher in the PSS group. In contrast to scintigraphic studies using semisolid meals gastric emptying of the copper pellet in PSS was accelerated. A general malabsorption of primary bile acids was not found. Prolonged colonic transit times correlate well with frequently complained obstipation. Gastric hypacidity could be the reason of elevated gastrin levels. The high motilin-levels in PSS could be due to a lack of the feed-back inhibition as a result of diminished phase-III activity of the interdigestive migrating motor complex. The elevation of CCK-levels could reflect compensation of neurogenic or myogenic disturbances of gallbladder contraction.