In order to elucidate mechanisms of protein plug formation, histochemical studies were performed on aggregates and protein plugs present in pancreatic juice. Pancreatic juice was obtained from three control subjects and five patients with chronic pancreatitis through endoscopic retrograde catheterization of the papilla. Specimens for staining were prepared in two ways: (1) fixed with 10 per cent formaldehyde, embedded in paraffin and sectioned, and (2) placed on slide glass and fixed with isopropylalcohol. Staining included hematoxylin-eosin, periodic-acid Schiff, von Kossa, alcian blue, toluidine blue and double staining with PAS and AB. The process of protein plug formation can be as follows: (1) a prerequisite for aggregate formation, consisting of clusters of desquamated epithelial cells, highly concentrated sulfated acidic mucopolysaccharide and neutral mucopolysaccharide, (2) formation of aggregates in which epithelial cells and amorphous substance are interlaced with developing fine reticular substance, (3) enlargement of aggregates by fusion with adjacent aggregates through bridging action of the reticular substance sprouting, like prickles, from their surface, and (4) "maturity" of aggregates, taking a three-dimensional form which result in a spherical, spheroidal or cylindrical protein plug.

To elucidate early biochemical changes of pancreatic juice and their reversibility in chronic alcoholics, pure pancreatic juice was collected from 23 chronic alcoholics by endoscopic retrograde catheterization of the papilla. Samples were collected at 1 minute intervals for 20 minutes after intravenous injection of secretin (Eisai, 1 U/kg) and for 10 minutes after CCK-PZ injection (Boots, 1 U/kg). Volume, bicarbonate concentration, protein concentration and three hydrolases were determined. Following results were obtained. (1) Five patients showed hypersecretory state. Four of the five patients showed hyperconcentration of protein. (2) Seventeen patients showed hyposecretory state. Lipase secretion was most frequently affected (94%). Maximal bicarbonate concentration was the next to be affected (82%). Amylase and chymotrypsinogen secretion were less frequently affected (65%). Flow rate was least frequently affected (24%). (3) It was suggested that exocrine dysfunction in chronic alcoholics is reversible in an early stage and that sequence of events with advancement of the stage is hypersecretion, hyperconcentration of protein, normalization of water secretion with a decrease in lipase secretion and maximal bicarbonate concentration, a decrease in amylase and chymotrypsinogen output, and finally a decrease in flow rate.

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Calcium concentration in human pure pancreatic juice was determined during wash-out period, secretin stimulation and pancreozymin stimulation. Specimens were collected by endoscopic retrograde catheterization of the papilla at one minute intervals for 20 minutes after intravenous injection of secretin (Eisai, 1 U/kg) and for 10 minutes after pancreozymin injection (Boots, 1 U/kg). The determination was also made in duodenal juice obtained during the ordinary pancreozymin-secretin test. Calcium concentration in duodenal juice was significantly raised in patients with chronic pancreatitis (suspected, definite or calcifying), confirming the results of previous investigators. Calcium concentration and calcium per mg of protein in human pure pancreatic juice were significantly raised in patients with chronic pancreatitis (suspected, definite or calcifying). Calcium per mg of protein in normal human pure pancreatic juice was quite similar to that reported in zymogen granules of the guinea-pig pancreas. Calcium output in human pure pancreatic juice was also significantly raised in patients with suspected chronic pancreatitis; it was within normal limits in patients with definite or calcifying chronic pancreatitis due to decreased volume output. Significance of these findings were discussed in relation to pathogenesis and early detection of chronic pancreatitis.

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