Paolo Casanova

Inhibitory Effect of Atropine on Cholecystokinin-Induced Gallbladder Contraction in Man

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) X kg-1 X min-1. In the other series of tests, an infusion of a low dose of atropine, 5 micrograms X kg-1 X h-1, was added to the hormone infusion. The smallest dose of CCK which significantly contracted the gallbladder was 0.0042 IDU X kg-1 X min-1. The highest dose of CCK infused, 0.0168 IDU X kg-1 X 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 X kg-1 X min-1, and partially inhibited (by 52%) the response to the highest dose. In 2 subjects in whom a higher dose of atropine, 15 micrograms X kg-1 X 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.

The sonographic appearance of the normal gastric wall: An in vitro study

In order to evaluate the real number and anatomical correspondence of the ultrasonographically recognizable layers within the gastric wall, we used a high frequency (7.5 MHz) rotating transducer to examine five surgical specimens of the stomach suspended in a water bath. Five layers were always clearly distinguishable within the gastric wall, whose thickness was 3-6 mm. Fine needles and lancets were localized at the level of the 3rd hyperechoic layer when inserted in the submucosa and in the 4th hypoechoic layer when inserted in the muscolaris propria. Thin echogenic bands were always displayed on both sides of other homogeneous tissues (spleen, myometrium) suspended in water. On the basis of these findings and also taking in account the physical laws of ultrasound interactions with tissues, we conclude that the 1st and the 5th hyperechoic layers are partially generated by ultrasound reflection at the interface liquid/wall. The 2nd hypoechoic layer corresponds to the deepest part of the mucosa; the 3rd hyperechoic to the submucosa and the submucosa/muscularis propria interface and the 4th hypoechoic layer to the muscularis propria.

Effect of somatostatin and thyrotropin-releasing hormone on cholecystokinin-induced gallbladder emptying

The effect of somatostatin (0.05 and 1.5 μg/kg/hr) and of thyrotropin-releasing hormone (0.1 and 1.0 μg/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 μg/kg/hr) of somatostatin on resting gallbladder volume was also evaluated. Somatostatin, at the dose of 0.05 μg/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 μg/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.

Effect of secretin on portal venous flow.

In this study we evaluated the effect of two different doses of secretin on portal haemodynamics (by pulsed Doppler associated with real time ultrasound) in 24 healthy humans. In 12 subjects (group A) we administered an intravenous dose of 75 clinical units of secretin and in the remaining 12 (group B) a dose of 20 CU. In all subjects the following parameters were studied before, during, and for 10 minutes after secretin administration: (a) calibre of the portal vein, (b) mean velocity of portal venous flow, and (c) volume of portal venous flow. In three subjects in each group we also evaluated the changes in flow in the superior mesenteric artery. Secretin injection induced a slight increase in both groups in comparison to basal values of portal vein calibre (mean of maximal per cent increase +25% in group A, not significant, and +16.7% in group B, not significant) and a noticeable increase of mean velocity (mean of maximal per cent increases +61.4% in group A, p less than 0.005, and +65.4% in group B, p less than 0.01) and flow volume (mean of maximal per cent increase +127% group A, p less than 0.005, and +114% group B, p less than 0.005). The magnitude of the haemodynamic changes did not differ significantly between the two groups. Doppler investigation of the superior mesenteric artery showed a marked increase of flow velocity (mean of maximal per cent increase +218% in group A and +246% in group B) and flow volume (mean of maximal per cent increase +276% in group A and +311% in group B). These data suggest that secretin has an appreciable vasoactive effect and induces a significant increase in portal venous flow even at doses much lower than those necessary for a maximal stimulation of exocrine pancreatic secretion.

Ultrasound detection of unusual spontaneous portosystemic shunts associated with uncomplicated portal hypertension.

Seven cases of unusual spontaneous portosystemic shunts observed by ultrasonography in the last 8 months are reported, including cases of coronary vein varicocele and patent umbilical vein; two cases of spleno‐retroperitoneal anastomosis; omphalo‐ilio‐caval anastomosis; superior mesenteric vein‐inferior vena cava anastomosis; spleno‐renal anastomosis; and spleno‐portal anastomosis and anastomosis from the splenic vein to the abdominal wall. One of these collateral vessels was also analyzed by pulsed Doppler flowmetry. The patients were either cirrhotic or had pre‐hepatic portal hypertension (resulting from chronic pancreatitis) and gave no history of gastrointestinal bleeding or ascites. Two of these patients had previously undergone surgery for problems associated with cholestasis. In both cases, presurgical sonographic studies were used to guide the surgical procedures in the hope of preserving the anomalous connections. Furthermore, ultrasound detection of spontaneous portosystemic shunts was an important factor in interpreting the clinical symptoms of these patients.

A case of aneurysm of the splenic artery visualized by dynamic ultrasonography

The possibility of using ultrasound to visualize the coeliac axis and its main branches, the splenic and common hepatic arteries, has already been extensively documented (Carlsen and Filly, 1976; Filly and Carlsen, 1976; Goldberg and Perlmutter, 1977; Skolnick and Royal, 1976). Using real time equipment we have identified a spherical echo-free space close to the origin of the splenic artery in a patient with undiagnosed abdominal pain. The ultrasound findings led us to suspect the presence of an aneurysm, which was subsequently confirmed, and surgical removal relieved the patients symptoms. We are unaware of any other previous case report of a similar aneurysm diagnosed by ultrasound, with the exception of a mycotic aneurysm of the hepatic artery (Sukerkar, 1977).

Improvement of pancreatic ultrasound imaging after secretin administration

The pancreas is usually well recognized by ultrasound, but in some cases it is obscured by the presence of gas in the stomach and duodenum. Water and other orally administered fluids produced poor results. In this study we stimulated pancreatic juice secretion by a standard dose of intravenous secretin in 24 normal subjects, and continuously monitored the pancreatic region for a period of 20 min. Four to five minutes after hormone administration pancreatic juice outflow into the duodenum generated a fluid-filled echofree area around the head of the pancreas, allowing excellent visualization of its boundaries and other channel structures (distal common bile duct, pancreatic duct and gastroduodenal artery). This method should be utilized in selected patients whenever a pathological condition of the pancreatic head region is suspected.