Human cholecystitis is associated with increased gallbladder prostaglandin I2 and prostaglandin E2 synthesis

• Published in: Hepatology (Baltimore, Md.) Md.), 1992-11, Vol.16 (5), p.1176-1179
• Main Authors: Myers, Stuart I., Bartula, Lori
• Format: Article
• Language: English
• Subjects: 6-Ketoprostaglandin F1 alpha - biosynthesis; Arachidonic Acid - metabolism; Biological and medical sciences; Cholecystitis - metabolism; Dinoprostone - biosynthesis; Epoprostenol - biosynthesis; Gallbladder - drug effects; Gallbladder - metabolism; Gallbladder - ultrastructure; Gastroenterology. Liver. Pancreas. Abdomen; Humans; Indomethacin - pharmacology; Intracellular Membranes - metabolism; Liver. Biliary tract. Portal circulation. Exocrine pancreas; Medical sciences; Microsomes - metabolism; Other diseases. Semiology
• ISSN: 0270-9139; 1527-3350
• DOI: 10.1002/hep.1840160512

Microsomal prostanoid synthesis was compared in normal gallbladders removed during organ donation and inflamed gallbladders removed at cholecystectomy. Normal human gallbladder microsomes demonstrated low rates of conversion of [14C]arachidonic acid to total labeled prostanoids, which increased during 1 to 30 min of incubation. Normal human gallbladder microsomes converted labeled substrate to all primary prostaglandins without demonstration of a major product. Inflamed human gallbladder microsomes increased the rate of conversion of [14C]arachidonic acid to total labeled prostanoids two or three times over the levels demonstrated by normal gallbladder microsomes at all times of incubation (p < 0.01). The main prostanoids synthesized by the inflamed human gallbladder microsomes were prostaglandin E2 and 6‐keto‐prostaglandin F1α, which were increased four times over the levels demonstrated by normal gallbladder microsomes (p < 0.01). These data showed that inflammation of the human gallbladder was associated with increased synthesis of gallbladder 6‐keto‐prostaglandin F1α, and prostaglandin E2. (HEPATOLOGY 1992;16:1176–1179.)