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

Authors

  • Stuart I. Myers M.D.,

    Corresponding author
    1. Department of Surgery, The University of Texas Medical School at Houston, Houston 77030
    2. Department of Surgery, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235–9031
    • Department of Surgery, The University of Texas Southwestern Medical School, 5323 Harry Hines Blvd., Dallas, TX 75235–9031
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  • Lori Bartula

    1. Department of Surgery, The University of Texas Medical School at Houston, Houston 77030
    2. Department of Surgery, University of Texas Southwestern Medical Center at Dallas, Dallas, Texas 75235–9031
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Abstract

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 F, 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 F, and prostaglandin E2. (HEPATOLOGY 1992;16:1176–1179.)

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