Abnormalities of gallbladder muscle associated with acute inflammation in guinea pigs

Muscle strips from experimental acute cholecystitis (AC) exhibit a defectiv e contraction. The mechanisms responsible for this impaired contraction are not known. The present studies investigated the nature of these abnormalit ies. AC was induced by ligating the common bile duct of guinea pigs for 3 d ays. Contraction was studied in enzymatic dissociated muscle cells. Cholecy stokinin (CCK) and prostaglandin E-2 (PGE(2)) receptor binding studies were performed by radioreceptor assay. The levels of lipid peroxidation, choles terol, phospholipid, and H2O2 as well as the catalase and superoxide dismut ase (SOD) activities were determined. PGE(2) content was measured by radioi mmunoassay. Muscle contraction induced by CCK, ACh, or KCl was significantl y reduced in AC, but PGE(2)-induced contraction remained normal. GTP gammaS , diacyglycerol (DAG), and 1,4,5-trisphosphate (IP3), which bypass the plas ma membrane, caused a normal contraction in AC. The number of functional re ceptors for CCK was significantly decreased, whereas those for PGE(2) remai ned unchanged in AC. There was a reduction in the phospholipid content and increase in the level of lipid peroxidation as well as H2O2 content in the plasma membrane in AC. The PGE(2) content and the activities of catalase an d SOD were also elevated. These data suggest that AC cause damage to the co nstituents of the plasma membrane of muscle cells. The preservation of the PGE(2) receptors may be the result of muscle cytoprotection.