We have studied the effect of atropine on cholecystokinin (CCK)-induced gallbladder contraction in 7 healthy volunteers by means of real-time ultrasonography. Two series of tests were carried out in random order and on separate days. In one series of tests, CCK alone was infused for 4 successive 15-min periods at sequentially increasing doses of 0.0021, 0.0042, 0.0084, and 0.0168 Ivy dog units (IDU·kg^-1·min^-1. In the other series of tests, an infusion of a low dose of atropine, 5 μg·kg^-1 •h^-1, was added to the hormone infusion. The smallest dose of CCK which significantly contracted the gallbladder was 0.0042 IDU· kg^-1·mm^-1. The highest dose of CCK infused, 0.0168 IDU·kg^-1·min^-1, produced almost total contraction of the organ. In all subjects, the infusion of atropine completely blocked the gallbladder response to 0.0042 and 0.0084 IDU·kg^-1 •min^-1, and partially inhibited (by 52%) the response to the highest dose. In 2 subjects in whom a higher dose of atropine, 15 μg• kg^-1 •h^-1, was tested, gallbladder contraction was totally abolished, even when the largest dose of CCK was infused. Contrary to what is generally believed, the results indicate that the response of human gallbladder to CCK is largely dependent on cholinergic innervation.

and variations in the interpretation of the ultrasound feature of the normal upper and lower GI tract wall. Scand J Gastroenterol 1986, 2l(suppl 123), 16-26 The aim of this study was to define the various ultrasound appearances of the normal upper and lower GI tract wall and to discuss current interpretations of the relationship between each echographic layer with the real anatomical structures. We studied a total of 70 patients by means of endoscopic ultrasonography and examined in vitro some surgical specimens of the normal stomach, colon and rectum. We found a 'five layer' structure at the level of the esophageal and gastric wall. This pattern was not recognized in the duodenum during the in vivo study. Our experimental results support the hypothesis that the first and fifth hyperechoic layers of the gastric wall are partially generated by ultrasound reflection at the interface liquid/wall and that the second hypoechoic layer corresponds to the deepest part of the mucosa. Important variations in the thickness of each layer were found in different conditions during in vivo studies. The fourth hypoechoic layer becomes very thin after water distension of the stomach. The in vitro investigation of the specimen of normal colon and rectum showed some different features. At this level it is sometimes possible to distinguish a separate very thin hypoechoic layer in the deepest part of the second layer, probably corresponding to the muscularis mucosae. The muscular layer is sharply divided into two distinct layers related to the circular and longitudinal muscular coats.

The effect of somatostatin (0.05 and 1.5 micrograms/kg/hr) and of thyrotropin-releasing hormone (0.1 and 1.0 microgram/kg/hr) on cholecystokinin-induced gallbladder emptying was studied in healthy volunteers by means of real-time ultrasonography. In addition, the action of increasing doses (0.05, 0.15, 0.45, and 1.35 micrograms/kg/hr) of somatostatin on resting gallbladder volume was also evaluated. Somatostatin, at the dose of 0.05 microgram/kg/hr (shown to produce blood levels similar to those measured after a meal) significantly inhibited the gallbladder contraction in response to cholecystokinin. Kinetic analysis showed that the interaction of somatostatin and cholecystokinin is of the noncompetitive type. The higher dose of the peptide (1.5 microgram/kg/hr) completely suppressed cholecystokinin-induced gallbladder contraction. In experiments carried out using somatostatin alone, a progressive increase in gallbladder volume in response to increasing doses of peptide was observed. The administration of either dose of thyrotropin-releasing hormone did not affect gallbladder emptying in any of the subjects studied. It is concluded that somatostatin is a potent inhibitor of cholecystokinin action on the gallbladder. The clear effectiveness of a very low, presumably physiological, dose indicates that somatostatin may play a physiological role in the regulation of gallbladder motor activity and provides further evidence that the peptide may act as a true hormone in man. Thyrotropin-releasing hormone does not seem to affect gallbladder motility, at least under the experimental conditions of the present study.