PubMed Health⌕ Search

Biomedical subjects

M J Ruwart

Publications and source records attributed to M J Ruwart.

16 recordsLinked to original sources
PubMed1979

Ionic composition of small intestinal secretion induced by PGE2.

Small intestinal fluid secretion induced by oral prostaglandin E2 in fasted rats was analyzed for various ionic components. Rat intestinal fluid had elevated calcium and potassium as well as decreased sodium and chloride concentrations relative to plasma electrolytes. Either low dose prostaglandin (0.15 mg/kg) or 1 ml of intragastric mannitol (5%) induced accumulation in the small intestine of fluid that had elevated chloride and depressed calcium and sodium concentrations compared to vehicle-treated controls. Higher doses of prostaglandin (1.0 mg/kg) led to secretions with increased sodium and chloride concentrations with respect to mannitol-induced fluid. Electrolyte concentrations in fluid induced by low dose prostaglandin appear to be similar to those in fluid caused by osmotically-induced changes. Higher doses of prostaglandin E2 induce additional electrolyte alterations which may result from modified gut transport of water and ions.

Animals↗
PubMed1979

The effects of synthetic prostaglandin analogs on canine hepatic bile flow.

The synthetic prostaglandin analogs 16, 16-dimethyl PGF2 alpha and 16, 16-dimethyl PGE2 were administered to dogs with chronic biliary and gastric fistulas. The effects of 16, 16 diMePGF2 alpha and 16, 16 diMePGE2 were evaluated on bile flow and composition and bile adenosine 3', 5' monophosphate (cyclic AMP) secretion. 16, 16 diMePGF2 alpha in doses of 0.125 and 0.25 microgram-kg-min significantly increased hepatic bile flow. The choleresis was characterized by increased chloride and bicarbonate secretion. Measurement by radioimmunoassay of bile cyclic AMP concentration demonstrated no evident increase in bile cyclic AMP secretion associated with the choleresis produced by 16, 16 diMePGF2 alpha. The administration of 16, 16 diMePGE2 in a dose range 0.01 to 1.0 microgram-kg-min did not significantly alter bile flow rates or composition. Bile erythritol-14C clearance, a measure of canalicular bile flow, was significantly increased by PGF2 alpha but not by 16, 16-dimethyl PGF2 alpha, suggesting that the mechanism of action of PGF2 alpha in stimulating hepatic bile flow may be different from that involved in 16, 16-dimethyl PGF2 alpha choleresis. The results of this study indicate that the synthetic PGF2 alpha analog produces a choleretic response not mediated by adenylate cyclase and associated with increased chloride and bicarbonate secretion.

16,16-Dimethylprostaglandin E2↗
PubMed1979

Naloxone inhibits the anti-diarrhoeal activity of loperamide.

1 Subcutaneous prostaglandin E2 (2.5 mg/kg) produces profuse diarrhoea in fed rats. 2 Pretreatment of rats with subcutaneous loperamide (1.0 mg/kg) completely prevents prostaglandin-induced diarrhoea. If naloxone is administered prior to loperamide injections the activity of the antidiarrhoeal compound is completely destroyed. 3 These data provide strong evidence that the antidiarrhoeal activity of loperamide is mediated via the opiate receptor.

Animals↗
PubMed1977

Evidence for additional mediator in prostaglandin-induced choleresis.

PGA1 and PGF2alpha were administered to isolated perfused porcine and canine livers to determine whether these hormones could induce hepatic choleresis. PGA1 (25 microgram/kg/10 min) decreased portal venous resistance, but had no effect on bile flow, oxygen, pyruvate, or lactate consumption in canine livers. PGF2alpha increased portal venous resistance and weight gain while decreasing bile flow and oxygen consumption in canine livers. At high doses (50 microgram/kg/10 min) these effects resulted in irreversible outflow block. At low doses (5 microgram/kg/10 min) these trends were reversible. Porcine livers did not exhibit the outflow block syndrome after PGF2alpha administration (100 microgram/kg/10 min); however, choleresis was not observed. Thus, the in-vivo choleretic effects of prostaglandins previously reported are probably mediated partially or wholly by extrahepatic release of other hormones, neurological stimulation or alterations in mesenteric blood flow.

Animals↗
PubMed1977

Structure-function relationships of peptide fragments of gastrin and cholecystokinin.

This study evaluates the structure-function relationships of the C-terminal peptide fragments of gastrin and cholecystokinin (CCK) in the biliary system and the stomach. Dogs with chronic biliary and gastric fistulas were used. Administration of the common fragments of CCK and gastrin with four and five amino acids and the active fragments of CCK with six through eight amino acids without sulfation of tyrosine in position 7 failed to alter hepatic bile flow from control values while significantly stimulating gastric hydrogen ion output. Administration of the seven and eight amino acid peptide fragments of CCK with sulfation of tyrosine in position 7 significantly increased hepatic bile flow. Administration of the sulfated octapeptide with 4 microgram/kg per h of nonsulfated octapeptide did not result in the inhibition of the choleresis produced by the sulfated peptide. The gastric hydrogen ion response produced by the administration of the nonsulfated and sulfated peptide was equal to that of the nonsulfated peptide alone. These results suggest that in the biliary system the receptor is highly specific as sulfation of the peptide fragment of CCK is essential for combining with the receptor, whereas in the stomach the receptor has little specificity and combines with all of the peptide fragments evaluated.

Animals↗
PubMed1976

Effect of the histamine (H2) inhibitor metiamide on histamine-stimulated bile flow in dogs.

The effects of the histamine H2-receptor inhibitor metiamide on histamine-stimulated canine bile flow and gastric hydrogen ion output were evaluated. Histamine was found to stimulate bile volume in doses comparable to those that stimulated gastric hydrogen ion output; both responses appeared to have the same maximal response dose, 150 mug/kg per h. Metiamide alone did not alter hepatic bile flow. Administration of metiamide, 2 mg/kg per h, along with various doses of histamine demonstrated that the H2-receptor antagonist decreased bile volume and gastric hydrogen ion output from values obtained with histamine administration alone. The D50 of histamine for bile flow was 16.3 mug/kg per h and the D50 for hydrogen ion output was 44.2 mug/kg per h, Kinetic analysis suggests that the decrease in histamine-stimulated hydrogen ion output produced by metiamide is the result of competitive inhibition; the decrease in histamine-stimulated bile volume by metiamide which is different from the hydrogen ion inhibition, suggests noncompetitive inhibition. These data indicate that the mechanism of histamine choleresis is different from the mechanism of histamine-stimulated gastric acid output and that histamine-stimulated bile flow may not be the result of direct hormone-receptor interaction.

Animals↗
PubMed1976

Use of automated, on-line pyruvate analysis.

Normothermic blood perfusions of isolated canine liver were undertaken to determine the most sensitive and reliable indicators of viability. Perfusate flow rates and arterial and portal venous pressures were monitored. Arterial and venous concentrations of potassium, pyruvate, serum glutamic oxaloacetic transaminase, and oxygen were monitored and the values stored on magnetic tape for computerized calculation of outputs. Continuous evaluation of taurocholate concentration in the perfusate allowed adjustment of infusion rate to provide a constant flow of bile across the hapatocytes. Pyruvate output, portal venous resistance, serum glutamic oxaloacetic transaminase output and potassium output provided the earliest indices of deterioration. Bile flow and oxygen consumption remained constant until irreversible outflow block had occured. The earliest and most constant parameter signaling deteoration of the ex vivo liver was pyruvate output. The deteriorating liver released pyruvate into the perfusate, while the functioning organ consumed or maintained the available substrate. Since pyruvate output occurs before the onset of irreversible damage, measures can be enacted to reverse the deterioration. Restoration of the preparation can be evaluated through the cessation of pyruvate output.

Animals↗
PubMed1975

Membrane properties of Thermoplasma acidophila.

Plasma membranes were isolated from Thermoplasma acidophila, a mycoplasma-like organism which grows optimally at pH 2 and 59 degrees. Cells in concentrated suspensions were lysed by titrating to pH 9.3. The membranes were purified by washing at pH 10 and centrifuging in a discontinuous sucrose gradient. Membrane purity was assessed by electron microscopy, determination of deoxyribonucleic acid content, polyacrylamide gel electrophoretic behavior. Gel patterns and amino acid composition of cells and membranes were found to differ significantly. The lipid contained small amounts of fatty acid esters and larger amounts of branched long-chain alkyl ethers.

Amino Acids↗
PubMed1975

Effect of glucagon on secretin-stimulated bile flow.

The effect of glucagon on secretin-stimulated bile flow was evaluated in dogs with chronic biliary and gastric fistulas. Evaluation of the effects of secretin and glucagon alone on hepatic bile flow indicated that the calculated maximal response (CMR) values of the two agents were similar. Secretin increased the bicarbonate concentration in hepatic bile whereas glucagon did not, suggesting basic differences in mechanism of action. Administration of glucagon to secretin-stimulated bile flow produced an increase in bile flow while decreasing the bicarbonate concentration in secretin-stimulated bile. Since the maximal response for bile flow to glucagon and secretin was significantly greater than the maximal response to either agent alone, glucagon produced potentiation of secretin-stimulated bile. Glucagon increased the CMR value of secretin-stimulated bile from 513 mul/min for secretin alone to 692 mul/min for secretin and glucagon. This was associated with no significant change in the values of the respective D50S. These data suggest that glucagon produced a noncompetitive augmentation of secretin-stimulated bile flow and suggest that the two agents do not utilize the same receptor to stimulate bile flow.

Animals↗