The behaviour of prostanoids during the course of acute experimental pancreatitis in rats

Abstract

The behavior of two vasoactive prostanoids was studied in experimental acute pancreatitis (AP) in rats. The stable metabolites of prostacyclin (PGI2) and thromboxane A2 (TXA2), 6-keto-PGF1 alpha and TXB2, respectively, were measured during the course of experimental AP. Blood samples were taken at 3, 6, and 8 h after the induction of AP. In AP both plasma 6-keto-PGF1 alpha plasma TXB2 and serum TXB2 increased up to 6 h simultaneously (6-keto-PGF1 alpha from 271.1 +/- 77.2 pg/ml (mean +/- SD) to 459.4 +/- 192.6 pg/ml, plasma TXB2 from 752 +/- 350 pg/ml to 3640 +/- 2160 pg/ml and serum TXB2 from 22.3 +/- 14.8 micrograms/ml to 140.8 +/- 52.8 micrograms/ml). After 6 h 6-keto-PGF1 alpha remained elevated, whereas serum TXB2 dropped significantly. We suggest that in AP the balance of PGI2 and TXA2 is initially maintained, but later on an imbalance appears to favor vasodilatory PGI2. These agents may contribute to the regulation of the blood flow in the pancreas and thus play a role in the pathophysiology of AP.

Prostacyclin Is Released Mainly from the Splanchnic Region during the Early Phase of Acute Experimental Hemorrhagic Pancreatitis in Dogs

“…The liberated PGH during AHP has been previously suggested to be of pancreatic origin [ 1 ], but there are also other organs rich in prostanoids, such as the lungs and kidneys, which may release the elevated prostanoid lev els measured in peripheral blood samples as has been reported earlier in this context [1][2][3]. It is obvious, how ever, that PGI2 measured in the blood samples collected from the portal vein in the present study was liberated mostly from the pancreas, as splenectomy was per formed prior to the induction of AHP to exclude the release of prostaglandins from that origin [10].…”

“…They are va soactive prostanoids and their plasma levels in systemic circulation have recently been reported to be elevated in different models of experimental acute pancreatitis [1][2][3]. The role of vasoactive substances in acute pancreati tis is not clear, but it has been proposed that they con tribute to pancreatic shock [4,5].…”

“…The role of vasoactive substances in acute pancreati tis is not clear, but it has been proposed that they con tribute to pancreatic shock [4,5]. During experimental acute hemorrhagic pancreatitits (AHP), PGH and TXA2 have been reported to be released into the pancreatic venous blood [6], systemic circulation [1][2][3] and perito neal exudate [1,6], but the definite origin of released PGH and TXA2 in acute pancreatitis is, however, poorly known.…”

Significance of thromboxane A2 and prostaglandin I2 in acute necrotizing pancreatitis in rats

“…TXA2 is generated (fourfold increase) in rats with acute pancreatitis (4,5,15), although not in dogs (16). In these rats thromboxane levels are reduced by treatment with inhibitors of thromboxane synthesis of flunarizine (5).…”

“…This inhibition tends to improve survival time in ANP (5). Plasma 6-keto-PGFI~ (the bioconversion product of PGI2) levels are increased to a much lesser extent (60% increase) (4,15). PGI2 is an inhibitor of TXA2 production (2).…”