Perfusion studies were performed in 35 healthy volunteers to investigate further the secretory effect of prostaglandin E1 (PGE1), administered intraluminally, on the human jejunum. A perfusion system with a proximal occluding balloon and continuous aspiration of duodenal secretions was used. The influence of PGE1 (0.9 mug per kg per min) on glucose, fluid, and ion transport was entirely reproducible throughout a 6-hr perfusion experiment and was fully reversible 60 min after the end of PGE1 administration. The influence of ethacrynic acid (EA), aspirin (two agents previously reported to inhibit choleraic secretion), and furosemide was studied both on basal jejunal absorption and on PGE1-induced secretion of water and electrolytes. EA (2.5 mg per kg), administered in jejunal lumen, significantly reduced (P less than 0.001) the net secretory effect of intraluminal PGE1, and suppressed the PGE1-induced increase in plasma-to-lumen unidirectional flux of sodium. Intravenous or intraluminal aspirin (25 to 40 mg per kg) as well as intraluminal furosemide (1.5 mg per kg) did not modify the PGE1-induced secretion nor the basal absorption rates. Plasma immunoreactive levels of PGE1, calcitonin, and diverse gut hormones did not change significantly during PGE1-induced secretion. These results indicate that (1) aspirin, an inhibitor of prostaglandin synthesis, has no influence on the intestinal secretory effect of preformed PGE1; (2) EA, unlike furosemide, inhibits in man PGE1-induced jejunal secretion, an effect of EA similar to that observed in animals on cholera toxin- and cyclic AMP-mediated secretion.

Adult↗

PubMed1975

Pancreatic cholera (W.D.H.A. syndrome). Histochemical and ultrastructural studies.

Results of light and electron-microscopic studies of primary pancreatic tumor and of metastasis in a new case of Pancreatic Cholera (P.C.) are reported. The primary tumor but not the metastases, contained unusual, large cystic glandular formations, lined both by pancreatic-duct- and small-intestine-like epithelia and closely connected with the endocrine proliferation. A part from a few D-cells, the endocrine tumoral cells could not be identified by histochemical stainings. Their ultrastructural pattern, with small secretory granules (diameter less than 300 nm) and numerous cytoplasmic bunches of filaments, was very similar to that of gastric and duodenal D1-cells. Normal duodenal D1-cells have been said to produce gastric inhibitory peptide, a substance structurally and biologically similar to the vasoactive intestinal peptide actually secreted by the tumor. The normal histological appearance of gastric, gallbladder, jejunal, ileal, right and left colonic mucosae is consistent with the responsibility of the tumoral secretion in the impairment of gut functions in P.C.

Acute Kidney Injury↗

PubMed1975

Pancreatic cholera. Sudies on tumoral secretions and pathophysiology of diarrhea.

Tumoral secretions and pathophysiology of diarrhea were studied in 1 patient with pancreatic cholera. High concentrations of vasoactive intestinal peptide were found in both systemic blood and tumoral extracts, together with increased plasma levels of calcitonin and protaglandins E and Falpha. Gastric inhibitory peptide and gastrointestinal and pancreatic hormones were absent from the tumor, except for small amounts of glucagon, and their blood levels were normal. Decreased basal but normal pentagastrin-stimulated gastric acid secretion, normal basal and secretin-stimulated pancreatic secretion, increased volume of gallbladder bile with high bicarbonate, and low bile salt concentrations were observed, but the electrolyte content and flow rate of fluid passing the duodenojejunal junction were within normal limits. Small intestine was found to be the origin of the water and electrolyte fasting losses. Jejunum was the site of bicarbonate secretion. Jejunal glucose and leucine-stimulated water and sodium transports were also strikingly decreased, whereas the absorption rates of the sugar and amino acid were normal. Colon reabsorbed high amounts of water and sodium but increased potassium losses. Biological effects of vasoactive intestinal peptide may explain most of the patient's upper digestive secretion abnormalities and small intestinal function impairments, whereas secondary aldosteronism might explain the modified colonic function.

Adult↗

PubMed1975