Prostaglandin F2α and Prostacyclin Tissue Levels in Early Phases of Trypsin-Induced Acute Pancreatitis in Rats

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Abstract
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 which 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.

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