cholecystokinin and Escherichia-coli-Infections

The gastrointestinal tract is the source of numerous peptide hormones. Since the gut will be altered severely during prolonged general circulatory low flow states, the reactions of the gut hormones are of great interest. In this study 18 anesthetized pigs were put into shock states to get first informations about the changes of the plasma levels of cholecystokinin (CCK). 12 pigs (group I and II) were exposed to a general circulatory shock state by a 2-hr intravenous infusion of a sublethal dose of Escherichia coli endotoxin. 6 of them (gr. II) first received a gastroenterectomy apart from a small duodenal remnant proximal and distal to the papilla of Vater. The remaining 6 pigs (gr. III) suffered a severe hemorrhagic-hypovolemic shock over a 150-min period by arterial bleeding. Plasma CCK increased significantly (p less than 0.05) in the aorta (gr. I, II), the portal vein (gr. I, II), the superior caval vein (gr. I), and the internal jugular vein (gr. I) at the end of the 2-hr endotoxin infusion. In group II, the rise of CCK levels in the superior caval vein was also marked, but insignificant. The CCK-concentrations in the internal jugular vein were measured only in group I. By contrast, no changes in plasma CCK were seen in hemorrhagic shock (gr. III). Within each group plasma samples taken from the various blood vessels at identical time points showed no significant differences. Since the plasma concentrations of CCK remained unchanged during hemorrhagic shock, the release of CCK by E. coli endotoxin is not due to the general circulatory low flow state.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Animals; Cholecystokinin; Digestive System Physiological Phenomena; Endotoxins; Escherichia coli Infections; Female; Male; Shock, Hemorrhagic; Shock, Septic; Swine

Fat absorption was studied in 10 patients recovering from an episode of acute infectious gastroenteritis who failed to gain weight despite adequate caloric intake. Three patients restudied after clinical improvement and three other infants with failure to thrive, unrelated to gastrointestinal problems, served as control subjects. Fat balance studies during the ingestion of a formula containing long-chain fatty acids demonstrated significant degrees of steatorrhea in patients (mean CFA 70.6 +/- 10.7 compared to 90.3 +/- 2.4 in control subjects). The administration of a test meal demonstrated a marked deficiency of duodenal bile acid concentration and of fat incorporation into the micellar phase in patients. Fecal bile acid excretion was significantly increased in patients (mean 33.9 +/- 11.6 microM/kg/day) as compared to control subjects (mean 13.5 +/- 3.1 microM/kg/day). Bacterial overgrowth and abnormalities of the small intestinal mucosa were not constant. Ileal dysfunction and associated bile acid loss are possible causes of disturbed fat assimilation following acute intestinal infection in children.

Topics: Acute Disease; Bile Acids and Salts; Body Fluids; Cholecystokinin; Diarrhea, Infantile; Dietary Fats; Duodenum; Escherichia coli Infections; Feces; Gastroenteritis; Humans; Infant; Intestinal Absorption; Lipid Metabolism; Lipids; Malabsorption Syndromes; Micelles; Salmonella Infections; Salmonella typhimurium