Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0149520 (acute cholecystitis)
 2,784 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The arachidonic acid metabolites are recognized as important biochemical mediators of inflammation in a wide variety of disease processes. Also the ability to change prostaglandin formation by inhibition of prostaglandin synthetase activity with aspirin and other nonsteroidal anti-inflammatory agents is important in the treatment of many diseases with an inflammatory component. Although gallbladder disease is primarily related to the development of cholesterol stones, inflammation is an important contributor to the subsequent symptoms and accompanying illness. This research evaluates the formation of prostaglandins E and F by gallbladder tissue. Gallbladder mucosal cells and muscle tissue were maintained in tissue culture medium. Production of prostaglandins E and F was determined by quantitation by radioimmunoassay of these substances in culture media and mucosal cell and muscle tissue homogenates. Prostaglandin production by normal gallbladder tissue in a variety of species including man was consistently demonstrated in the nanogram per milligram mucosal cell or muscle tissue protein range. In cats, inflammation was produced by placing a 4% carrageenan-soaked sponge in the gallbladder, and prostaglandin synthetase inhibition was produced by indomethacin administration. The feline gallbladder increased prostaglandin F production in inflamed gallbladder mucosal cells and E production by inflamed gallbladder muscle tissue, and indomethacin inhibited these increases. A positive, significant correlation existed between the increased prostaglandin E and prostaglandin F production by inflamed gallbladder tissue and the amount of inflammation present as determined by a histologic score. The histologic score of the amount of gallbladder inflammation present was decreased significantly by indomethacin when compared with inflamed gallbladders from cats not receiving indomethacin. Prostaglandins may play a role in the inflammatory processes occurring in acute cholecystitis.
 ...
PMID:The role of prostaglandins in feline experimental cholecystitis. 404 47

The pathogenesis of acute cholecystitis (AC) is controversial. Bile acids may be involved in the pathogenesis of AC because the hydrophobic chenodeoxycholic acid (CDCA) reproduced in vitro the muscle dysfunction observed in AC and was prevented by the hydrophilic ursodeoxycholic acid (UDCA). The present study examined the in vivo effects of UDCA or CDCA on gallbladder muscle dysfunction caused by AC. Guinea pigs were treated with placebo, UDCA, or CDCA for 2 weeks before sham operation or induction of AC by bile duct ligation (BDL) for 3 days. Pretreatment with oral UDCA prevented the defective contraction in response to agonists (acetylcholine [ACh], cholecystokinin 8 [CCK-8], and KCl) that occurs after BDL. Prostaglandin (PG) E(2)-induced contraction remained normal in the placebo and UDCA-treated groups but was impaired in the CDCA-treated group. Treatment with UDCA also prevented the expected increase in the levels of H(2)O(2), lipid peroxidation, and PGE(2) content in the placebo-treated AC group, whereas CDCA caused further increases in these oxidative stress markers. The binding capacity of PGE(2) to its receptors and the activity of catalase were reduced after treatment with CDCA. Treatment with UDCA enriched gallbladder bile acids with its conjugates and reduced the percentage of CDCA conjugates. In contrast, treatment with CDCA significantly decreased the percentage of UDCA in bile. In conclusion, oral treatment with UDCA prevents gallbladder muscle damage caused by BDL, whereas oral treatment with CDCA worsens the defective muscle contractility and the oxidative stress.
 ...
PMID:Hydrophilic but not hydrophobic bile acids prevent gallbladder muscle dysfunction in acute cholecystitis. 1277 24