Prostanoid Imbalance in Experimental Acute Necrotizing Pancreatitis in Rats

Abstract

van Ooijen B, Kort WJ, Zijlstra FJ, Vincent JE, Wilson JHP, Westbroek DL. Prostanoid imbalance in experimental acute necrotizing pancreatitis in rats. Scand J Gastroenterol 1988, 23, 193–198

In an investigation of the pathogenesis of acute necrotizing pancreatitis (ANP) the plasma levels of TXB₂ 6-keto-PGF_1α and PGE₂ were measured in rats. After induction of ANP by injection of 5% sodium taurocholate into the pancreatic duct, a marked increase in TXB, levels and a slight increase in 6-keto-PGF_1α levels were found. PGE₂ levels decreased. Mortality was 100% within 30 h. Pretreatment with chloroquine, a phospholipase A₂ inhibitor, led to an inhibition of TXB, production, whereas 6–keto-PGF_1α and PGE, levels showed a surprising slight elevation in the first 6h. Pretreatment with chloroquine decreased mortality by 30%. Pretreatment with FPL 55712, a leukotriene synthesis blocker, caused an increase in TXB₂ and PGE, levels, whereas the formation of 6-keto-PGF_1α remained unaltered. Two out of nine animals survived after pretreatment with FPL 55712. The results of the present study indicate that arachidonate end products are involved in ANP. The significance of the high TXB, levels, decreased PGE, levels, and only slightly elevated 6-keto-PGF_1α levels during ANP requires further investigation. The thromboxane A₂ to prostacyclin ratio may be important.

Key Words:

• Acute necrotizing pancreatitis
• prostaglandins
• thromboxane A₂/prosta-cyclin ratio