dinoprost and Pancreatitis

Changes in endogenous pancreas production of prostaglandins D2, F2 alpha, E2, and E1 in early stages of acute necrotizing pancreatitis induced by intraductal administration of 3.5% sodium taurocholate have been determined by radioimmunoassay of chromatographically purified tissue extracts. For this purpose 18 male Wistar rats were randomized in three groups: control, pancreatitis, and pancreatitis plus indomethacin. Pancreas tissue samples were obtained 5 min after pancreatitis induction. In the pancreatitis-induced group, prostaglandins D2, F2 alpha, and E2 show significantly increased tissue levels relative to the controls whereas prostaglandin E1 remains unmodified. These results suggest a role for series 2 prostaglandins in the earlier stages of pancreatitis.

Topics: Acute Disease; Alprostadil; Amylases; Animals; Dinoprost; Dinoprostone; Hemorrhage; Indomethacin; Lipase; Male; Necrosis; Pancreas; Pancreatitis; Prostaglandin D2; Prostaglandins; Rats; Rats, Wistar; Taurocholic Acid

The content of pancreatic enzymes, cyclic nucleotides and prostaglandins (PG) in the duodenal contents was measured in 77 patients with chronic pancreatitis and in 20 healthy individuals. Pancreatitis exacerbation was attended by a decrease in enzymatic activity, in bicarbonate, cAMP and cGMP production. The content of PGE in pancreatic secretion remained normal, that of PGF2 alpha was elevated. Stimulation of the exocrine part of the pancreas by means of euphylline, pentagastrin and calcium was accompanied by the rise of the content of cyclic nucleotides rather than of PG. Suppression of enzymatic secretion by contrykal was followed by the reduction in the content of the cyclic nucleotides and PGE. The data suggest that cyclic nucleotides and PG are involved in the mechanism by which the external secretion of the pancreas is impaired in patients with chronic pancreatitis.

Topics: Adult; Amylases; Chronic Disease; Cyclic AMP; Cyclic GMP; Dinoprost; Female; Humans; Lipase; Male; Middle Aged; Pancreas; Pancreatic Juice; Pancreatitis; Prostaglandins E; Trypsin

Local variations of prostaglandin (PG) I2 and F2 alpha were studied in the pancreatic tissue during the first hour of an acute experimental necrohemorrhagic pancreatitis. The local pancreatitis was induced by trypsin injection into the interstitium of the splenic part of rat pancreas, and a saline injection was given into the interstitium in the duodenal part of the same pancreas as control. PGF2 alpha level was measured by specific radioimmunoassay (RIA), and the stable degradation product of PGI2, the 6-keto-PGF1 alpha, was determined also by RIA as an index of PGI2 level. The results were compared between the two regions and with control intact pancreata. The PGI2 level transiently decreased, whereas the PGF2 alpha increased in the region of localized hemorrhagic pancreatitis when compared with the intact pancreata. By contrast, the quickly disappearing edematous reaction induced by saline injection was accompanied by opposite changes in the two PGs studied: PGI2 was transiently elevated and PGF2 alpha diminished. In consequence, the ratio of the two PGs was shifted in favor of PGI2 in a transient edematous reaction and in favor of PGF2 alpha in hemorrhagic pancreatitis. It was concluded that PGI2 plays some protective role while PGF2 alpha might be one of the aggressive mediators in the inflammatory process. Their biological importance must be limited since PGF2 alpha alone did not induce pancreatitis nor did PGI2 protect against the trypsin-induced local pancreatitis.

Topics: Acute Disease; Animals; Dinoprost; Edema; Epoprostenol; Female; Kinetics; Pancreas; Pancreatitis; Prostaglandins E; Prostaglandins F; Rats; Reference Values; Trypsin