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H O Wheeler

Publications and source records attributed to H O Wheeler.

At least 19 recordsLinked to original sources
PubMed1989

Characterization of hormone-sensitive adenylate cyclase in rabbit gallbladder mucosa.

1. We have developed a plasma membrane preparation from the mucosal epithelium of rabbit gallbladder and have characterized the hormonal sensitivity of adenylate cyclase in this preparation. 2. Basal activity is low and is stimulated by GTP and GppNHp. Hormonal stimulation is largely dependent on exogenous guanine nucleotide. 3. Several prostaglandins (E1 approximately E2 greater than A1 greater than B1), vasoactive intestinal peptide and the beta-adrenergic agonist, isoproterenol, stimulate mucosal adenylate cyclase activity; a variety of peptides and neurotransmitters (secretin, cholecystokinin, arg-vasopressin, oxytocin, histamine, dopamine and serotonin) are without effect. 4. The data support the hypothesis that the inhibitory effect of prostaglandins, vasoactive intestinal peptide, and isoproterenol on gallbladder fluid absorption in certain species may be mediated by cyclic AMP. 5. The membrane preparation should be useful in further characterizing hormone receptor-transducer interactions of the gallbladder mucosal epithelium.

Adenylyl Cyclases↗
PubMed1975

The choleretic effect of iodipamide.

It is well established that a number of organic anions are excreted by the liver into bile in association with a marked increase in bile flow. Previous studies have shown that iodipamide (3,3'-(adipoyl-diimino)bis[2,4,6-triiodobenzoic acid]), the radiographic contrast material used for intravenous cholangiography, is a potent choleretic. Experiments were performed in unanesthetized dogs to determine if the increased bile flow produced by iodipamide is canalicular or ductular in origin, to quantitate the choleresis associated with iodipamide and taurocholate excretion, and to correlate these findings with the results of in vitro studies in which the osmotic activities of iodipamide and taurocholate in both isotonic saline and bile were determined. The plasma erythritol clearance increase linearly with the excretion of iodipamide, indicating that iodipamide stimulates canalicular bile flow. The choleretic potency of iodipamide (22 ml/mmol) is approximately 3 times that of taurocholate (7.8 ml/mmol), yet the osmotic activity of iodipamide in bile (1.5 mosmol/mmol) is only twice as great as that of taurocholate in bile (0.8 mosmol/mmol). It therefore appears that, per unit of effective osmotic solute secreted, iodipamide carries more water into the bile canaliculi than does taurocholate.

Animals↗
PubMed1975

Biliary excretion of iodipamide.

Conflicting data have been reported concerning the optimum dose and rate of administration of iodipamide required to obtain maximum radiographic opacification of the biliary tree during intravenous cholangiography. Experiments were performed in dogs to determine the effect of plasma concentration on the excretion and concentration of iodipamide in the bile and urine during a steady state of infusion and excretion. The data indicate that a hyperbolic relation exists between the plasma concentration and both the biliary concentration and the total biliary excretion. A mathematical expression of these relations is presented. At low plasma concentrations, iodipamide was not excreted in the urine. However, at high plasma concentrations, urinary excretion increased sharply. It appears that a biliary concentration of iodipamide sufficient to achieve adequate radiographic visualization of the biliary tree can be obtained without significant renal excretion by constant infusion of iodipamide at an appropriate rate in dogs. Stepwise increase in the infusion rate until adequate radiographic visualization is obtained may be the best method for performing intravenous cholangiography to obtain visualization with the least amount of iodipamide in order to minimize toxicity.

Animals↗
PubMed1972

Biliary excretion of lecithin and cholesterol in the dog.

The biliary excretion rates of bile acid, lecithin, and cholesterol were measured in unanesthetized dogs after interruption of enterohepatic circulation and during infusions of sodium taurocholate, sodium glycocholate, sodium dehydrocholate, SC2644 (a bicyclic organic acid with high choleretic potency), and secretin. Both lecithin output and cholesterol output were directly related to bile acid excretion rate. The curves describing these relationships were concave downward. Molar concentration ratios of lecithin-to-bile acid declined gradually from approximately 0.4 to 0.2 as bile acid output increased from approximately 1 to 70 mumoles/min. Cholesterol-to-lecithin molar ratios were highest (0.05-0.15) at very low rates of bile acid excretion, but descended rapidly to a plateau (0.03-0.04) which was constant over the entire range of bile acid excretion rates from 10 to 70 mumoles/min. Similar lipid excretion patterns were observed during glycocholate infusion, but secretin-induced choleresis and dehydrocholate-induced choleresis were unaccompanied by any increments in lecithin or cholesterol excretion and SC2644 (which caused a marked increase in canalicular bile production as measured by erythritol clearance) caused a depression of lipid excretion. The data are consistent with the view that lecithin moves passively from cell membranes to intracanalicular micelles, that transport of cholesterol is coupled to lecithin transport, and that there is also a small amount of independent passive transport of cholesterol from membranes to micelles. A model developed on these assumptions has been shown to behave in a fashion consistent with the entire range of these observations.

Animals↗
PubMed1966

Fluid transport in the rabbit gallbladder. A combined physiological and electron microscopic study.

The fine structure of the rabbit gallbladder has been studied in specimens whose functional state was undetermined, which were fixed either in situ or directly after removal from the animal; in specimens whose rate of fluid absorption was determined, either in vivo or in vitro, immediately prior to fixation; and in specimens from bladders whose absorptive function was experimentally altered in vitro. Considerable variation was found in the width of the epithelial intercellular spaces in the bladders whose functional state was undefined. In bladders known to be transporting fluid, either in vivo or in vitro, the intercellular spaces were always distended, as were the subepithelial capillaries. This distension was greatest in bladders which had been functioning in vitro. When either Na(+) or Cl(-) was omitted from the bathing media, there was no fluid transport across the wall of the gallbladder studied in vitro. The epithelial intercellular spaces of biopsies taken from several bladders under these conditions were of approximately 200 A width except for minor distension at the crests of mucosal folds. The addition of the missing ion rapidly led to the reestablishment of fluid transport and the distension of the intercellular spaces throughout most of the epithelium of these bladders. Studies of sodium localization (by fixation with a pyroantimonate-OsO(4) mixture) showed high concentrations of this ion in the distended intercellular spaces. Histochemical studies of ATPase activity showed that this enzyme was localized along the lateral plasma membrane of the epithelial cells. The analogy is drawn between the structure of the gallbladder mucosa and a serial membrane model proposed by Curran to account for coupled solute-solvent transport across epithelia. It is concluded that the intercellular compartment fulfills the conditions for the middle compartment of the Curran model and that active transport of solute across the lateral plasma membrane into the intercellular space may be responsible for fluid absorption by the gall bladder.

Adenosine Triphosphatases↗