Comparison of autoanalyzer and back titration for measurement of bicarbonate concentration in endoscopically collected pancreatic fluid.

Objectives: In secretin-stimulated pancreatic function testing, the standard technique for bicarbonate measurement is back titration (BT). Chemistry autoanalyzers (AAs) automate bicarbonate measurement and are universally available; however, this method has not been validated in pancreatic fluid. The aims of the study were (1) to compare the AA and BT for measurement of bicarbonate in pancreatic fluid and (2) to determine the effects of variable conditions on bicarbonate concentration.

Reactive oxygen species are messengers in maintenance of human and guinea pig gallbladder tonic contraction.

The tonic contraction of human and guinea pig gallbladder (GB) is dependent on basal levels of PGE(2) and thromboxane A(2) (TxA(2)). The pathway involved in the genesis of these prostaglandins has not been elucidated. We aimed to examine the source of reactive oxygen species (ROS) and whether they contribute to the genesis of GB tonic contraction by generating basal prostaglandin levels.

Role of caveolae in the pathogenesis of cholesterol-induced gallbladder muscle hypomotility.

Muscle cells from human gallbladders (GB) with cholesterol stones (ChS) exhibit a defective contraction, excess cholesterol (Ch) in the plasma membrane, and lower binding of CCK-1 receptors. These abnormalities improved after muscle cells were incubated with Ch-free liposomes that remove the excess Ch from the plasma membrane. The present studies were designed to investigate the role of caveolin-3 proteins (Cav-3) in the pathogenesis of these abnormalities.

Prostaglandins mediate tonic contraction of the guinea pig and human gallbladder.

The gallbladder (GB) maintains tonic contraction modulated by neurohormonal inputs but generated by myogenic mechanisms. The aim of these studies was to examine the role of prostaglandins in the genesis of GB myogenic tension. Muscle strips and cells were treated with prostaglandin agonists, antagonists, cyclooxygenase (COX) inhibitors, and small interference RNA (siRNA).

Nongenomic effects of progesterone on the contraction of muscle cells from the guinea pig colon.

Progesterone (PG) affects muscle cells by genomic mechanisms through nuclear receptors and by nongenomic mechanisms through unidentified pathways. This study aimed to determine the pathways mediating its nongenomic actions. Experiments were performed in dissociated muscle cells from guinea pig colons.

Role of progesterone signaling in the regulation of G-protein levels in female chronic constipation.

Background & Aims: Chronic constipation caused by slow transit is common in women with an F/M ratio of 9:1. The cause and mechanisms responsible for this syndrome are unknown. Progesterone has been suggested as a possible contributing factor.

Impaired cytoprotective function of muscle in human gallbladders with cholesterol stones.

Acute cholecystitis develops in gallbladders (GB) with excessive bile cholesterol (Ch). Increased membrane Ch content affects membrane function and may affect PGE(2) receptors involved in the cytoprotection against acute inflammation. This study was aimed at determining whether the cytoprotective response to PGE(2) is affected by lithogenic bile with Ch.

Role of PGE2 on gallbladder muscle cytoprotection of guinea pigs.

H2O2 and taurochenodeoxycholic acid (TCDC) impair the contraction induced by CCK-8, ACh, and KCl without affecting the actions of PGE2 and damage functions of membrane proteins except for PGE2 receptors. The aim of this study was to examine whether the preserved PGE2 actions contribute to cytoprotective mechanisms against reactive oxygen species. Muscle cells from guinea pig gallbladder were obtained by enzymatic digestion.

PAF-like lipids- and PAF-induced gallbladder muscle contraction is mediated by different pathways in guinea pigs.

H2O2 stimulates gallbladder muscle contraction and scavengers of free radicals through the generation of PGE2. Oxidative stress causes lipid peroxidation and generation of platelet-activating factor (PAF) or PAF-like lipids. The present studies therefore were aimed at determining whether either one induced by H2O2 mediates the increased generation of PGE2.

Hydrophilic but not hydrophobic bile acids prevent gallbladder muscle dysfunction in acute cholecystitis.

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.

Effects of bile acids on the muscle functions of guinea pig gallbladder.

Hydrophobic bile acids impair gallbladder emptying in vivo and inhibit gallbladder muscle contraction in response to CCK-8 in vitro. This study was aimed at determining the mechanisms of muscle cell dysfunction caused by bile acids in guinea pig gallbladders. Muscle cells were obtained by enzymatic digestion.

Reactive oxygen species (H(2)O(2)): effects on the gallbladder muscle of guinea pigs.

Reactive oxygen species (ROS) have been implicated in the pathogenesis of muscle dysfunction in acute inflammatory processes. The aim of these studies was to determine the effects of ROS on gallbladder muscle function in vitro. Single muscle cells were obtained by enzymatic digestion.