bluuebunny/crossref_metadata_2025_split huggingface dataset:
The Effect of the Cholecystokinin Antagonist Devazepide (L364718) on the Ileal Brake Mechanism in the Rat
Authors: Brown Nicola J , Rumsey R D E , Read N W 
Published: April 2011

Abstract
Studies were carried out on 28 male adult rats to investigate whether the selective cholecystokinin-receptor antagonist devazepide influences gastrointestinal transit under control conditions and when it is delayed by ileal infusion of lipid. Stomach-to-caecum transit time of the head of the test meal was measured using environmental hydrogen analysis and the distribution of the meal was assessed using the radiolabeled meal technique. Oral administration of devazepide (4 mg kg−1) had no significant effect on transit time of the head of the baked bean test meal under control conditions, but significantly reversed the delay in transit time induced by ileal infusion of lipid (P &lt; 0·01). Studying the distribution of the meal showed that Intralipid delayed transit time by delaying both gastric emptying (P &lt; 0·01) and small bowel transit (P &lt; 0·05). Devazepide did not alter the control distribution of the meal during ileal saline infusion, but during ileal infusion of lipid, devazepide further delayed gastric emptying (P &lt; 0·01); the geometric centre of the meal was situated more proximally in the gastrointestinal tract (P &lt; 0·05), but there was more of the meal in the colon (P &lt; 0·01). The latter is compatible with the early rise in environmental hydrogen during devazepide administration and ileal lipid infusion and suggests that peripheral cholecystokinin receptors may modulate or mediate the delay in small bowel transit induced by ileal lipid. However, the data also suggest that mechanisms other than those involving cholecystokinin play a dominant role in the regulation of postprandial and lipid-delayed gastric emptying of a meal.
Chemical Incompatibility Between Procainamide Hydrochloride and Glucose Following Intravenous Admixture
Authors: Sianipar A , Parkin J E , Sunderland V B 
Published: April 2011

Abstract
The chemical reaction between procainamide hydrochloride and glucose following admixture to glucose infusion has been investigated. Substantial amounts (10–15% after 10h at room temperature) of the procainamide is lost with the formation of a mixture of the corresponding α- and β-glucosylamines. The chemical identity of the latter compounds was confirmed by 13C and 1H nuclear magnetic resonance spectroscopy.
Distribution and Elimination of Sulphadimethoxine and Its Metabolites in Treated Chicken
Authors: Nagata Tomoko , Fukuda Yoshio 
Published: April 2011

Abstract
Sulphadimethoxine (SDM), and its metabolites, N4-acetyl SDM, N1-(2-methyl-6-hydroxy-4-pyrimidinyl) sulphanilamide (6-OH-SDM), N1-(6-methyl-2-hydroxy-4-pyrimidinyl) sulphanilamide (2-OH-SDM), N1-(2,6-dihydroxy-4-pyrimidinyl) sulphanilamide (2,6-diOH-SDM) and SDM N1-glucuronide in chicken tissues were extracted, partially purified by Bond Elute SCX cartridges, and assayed and identified by HPLC/LC-MS after administration of SDM to chickens. During the administration and 24 h after withdrawal, SDM and 6-OH-SDM were observed in almost all tissues and excreta. N4-Acetyl SDM and 2,6-diOH-SDM were observed in some tissues, but 2-OH-SDM and SDM N1-glucuronide were observed in a few limited tissues. Twenty four hours after withdrawal, SDM and its metabolites, except 6-OH-SDM, decreased. SDM and its metabolites were eliminated from all tissues within 48 h of withdrawal.
Curcuminoids as Potent Inhibitors of Lipid Peroxidation
Authors: Sreejayan  , Rao M N A 
Published: April 2011

Abstract
Earlier studies showed that curcumin is a potent inhibitor of iron-catalysed lipid peroxidation. Demethoxycurcumin, bisdemethoxycurcumin and acetylcurcumin were tested for their ability to inhibit iron-stimulated lipid peroxidation in rat brain homogenate and rat liver microsomes. Comparison of the results with curcumin showed that all compounds are equally active, and more potent than α-tocopherol. These results showed that the methoxy and phenolic groups contribute little to the activity. Spectral studies showed that all compounds could interact with iron. Thus, the inhibition of iron-catalysed lipid peroxidation by curcuminoids may involve chelation of iron.
Fenbufen Pretreatment Potentiates the Anticonvulsant Activity of CPPene and NBQX in DBA/2 Mice
Authors: De Sarro Giovambattista , Renne Stefania , Nava Felice , De Sarro Angela 
Published: April 2011

Abstract
The anticonvulsant activity of 3-((±)-2-carboxypiperazin-4-yl)-***l-propenyl-***l-phosphonic acid (CPPene) and 2,3-dihydroxy-6-nitro-7-sulphamoyl-benzo(F)quinoxoline (NBQX), two excitatory amino acid antagonists, was studied against audiogenic seizures in DBA/2 mice, following intraperitoneal (i.p.) or intracerebroventricular (i.c.v.) administration. Maximal anticonvulsant protection was observed 15–30 min following NBQX and 45–180 min after CPPene. Coadministration with fenbufen (20mgkg-1, i.p.), a non-steroidal anti-inflammatory agent, enhanced and prolonged the anticonvulsant actions of CPPene and NBQX and also potentiated and prolonged the impairment of rotarod performance. The enhancement of the anticonvulsant activity and the prolonged impairment of rotarod performance suggests that fenbufen may have some pharmacokinetic interactions with CPPene and NBQX and that fenbufen is able to increase the brain levels of these excitatory amino acid antagonists. In particular, fenbufen was able to exert a major degree of potentiation of effects of NBQX rather than those of CPPene, suggesting that the chemical structures of these excitatory amino acid antagonists are responsible for the different degree of interactions between CPPene or NBQX and fenbufen. NBQX appears to have a notable similarity with quinolones whilst CPPene does not. Additionally fenbufen may displace CPPene and NBQX from plasma binding sites or inhibit the renal excretion. The present data are also consistent with previous studies showing pharmacokinetic interactions between fenbufen and quinolones.
Upregulation of antithrombotic ectonucleotidases by aspirin in human endothelial cells in-vitro
Authors: Cheung Po Kam , Visser Jan , Barker Winston W 
Published: April 2011

Abstract
Ecto ATP-diphosphohydrolase (apyrase) activity of human endothelial cells following aspirin treatment has been studied in-vitro. It was shown by HPLC analysis of supernatant samples that pre-incubation of the cultures with aspirin resulted in a significantly increased turnover of supplemented ATP into its degradation products (ADP and AMP). Enhanced expression of ectoenzyme after aspirin treatment could be observed as demonstrated by immunofluorescence-staining with monoclonal anti-apyrase antibodies. This suggests enhancement of endothelial ATP-diphosphohydrolase activity induced by aspirin. The present data obtained in human vascular cells in-vitro are in line with results from previous animal studies in-vivo, suggesting a novel cyclo-oxygenase-independent antithrombotic activity of aspirin.
Incorporation of α-Tocopherol in Liposomes Promotes the Retention of Liposome-encapsulated Glutathione in the Rat Lung
Authors: Suntres Z E , Shek P N 
Published: April 2011

Abstract
The present study was undertaken to investigate whether α-tocopherol incorporated in liposomes could improve the retention of entrapped glutathione (GSH) in the lung following intratracheal instillation in rats. Rats were treated with a single dose of [3H]GSH entrapped in liposomes with or without 30 mol% α-tocopherol and killed 0, 24 or 48 h later. The retention of GSH in the lung was assessed by measuring the recovery of either 3H-label or GSH in the lung. Animals instilled with free [3H]GSH were found to retain only 2% of the administered dose at 24 h after treatment and no detectable radioactivity at 48 h. Liposome encapsulation altered the pulmonary retention of GSH with 18 and 10% of radioactivity remaining in the lung at 24 and 48 h post-treatment, respectively. The instillation of GSH encapsulated in α-tocopherol-containing liposomes resulted in the highest level of GSH retention in the lung, namely 37 and 30% of the administered GSH dose at 24 and 48 h, respectively. Results from Sepharose 4B column chromatography revealed that lung homogenates, obtained from rats instilled with GSH entrapped in α-tocopherol-containing liposomes, 24 and 48 h earlier, contained 2 eluted GSH-related components—one associated with the liposomal lipid marker in the void volume and the other as free GSH tripeptide, suggesting a slow sustained release effect mediated by the liposomal formulation. The same liposome preparation containing both α-tocopherol and GSH also conferred better protection against FeADP-induced lipid peroxidation than liposomes containing either α-tocopherol or GSH alone, indicative of a potentially effective antioxidant formulation for treating oxidative lung injury.
Ex-vivo and In-vivo Antithrombotic Effect of Triflavin, an RGD-containing Peptide
Authors: Sheu J R , Huang T F 
Published: April 2011

Abstract
Triflavin, an Arg-Gly-Asp-containing snake venom peptide, inhibits platelet aggregation through the blockade of fibrinogen binding to the activated platelets. It binds to fibrinogen receptors associated with the glycoprotein IIb/IIIa complex with a Kd value of 7 × 10−8 m. In this study, we found that 125I-triflavin reached the maximal binding to human platelets within 5 min at 25°C. In addition, when triflavin was intravenously administered at 1·0 mg kg−1 to rabbits, it reversibly impaired the platelet aggregation of platelet-rich plasma caused by ADP (20 μm) ex-vivo over 30 min. The platelet counts of the experimental rabbits remained unchanged. Triflavin was effective in reducing the mortality of ADP-induced acute pulmonary thromboembolism in mice when administered intravenously at a dose of 2 μg g−1. Therefore, triflavin was proven to be an effective antithrombotic agent in preventing ADP-induced acute pulmonary thromboembolism in mice and impairing reversibly the platelet function of rabbits when given intravenously.
The effect of colestipol and cholestyramine on the systemic clearance of intravenous ibuprofen in rabbits
Authors: El-Sayed Yousry M , Al-Meshal Mohamed A , Al-Angary Abdulaziz A , Lutfi Khalil M , Gouda M Wafik 
Published: April 2011

Abstract
The effect of oral administration of the non-absorbable anion-exchange resins cholestyramine and colestipol on the systemic clearance and other pharmacokinetic parameters of intravenously administered ibuprofen (25 mg kg−1) was studied in rabbits. Single doses of colestipol hydrochloride (0·4 g kg−1) or cholestyramine (0·17 g kg−1) were given 30 min before ibuprofen administration. In cholestyramine-treated rabbits a significant reduction in ibuprofen plasma concentration was observed compared with both control (water only) and colestipol-treated rabbits. Cholestyramine treatment resulted in a significant decrease in the terminal elimination half-life and the mean residence time. Furthermore, a 31% increase in the systemic clearance and 23% decrease in the area under the plasma concentration-time curve were also observed in cholestyramine-treated rabbits. Colestipol treatment did not change these parameters. The volume of distribution parameters (Vdss and Vdarea) did not change following either treatment. The changes in the pharmacokinetic parameters are compatible with an acceleration of ibuprofen elimination induced by oral administration of cholestyramine and not by colestipol. This effect is thought to be due to augmentation of net biliary excretion through enteric binding.
Location of Probucol in Lipoproteins Inferred from Compositional Analysis of Lipoprotein Particles. An In-vitro Study
Authors: Bard Jean-Marie , Urien Saîk , Fruchart Jean-Charles , Tillement Jean-Paul 
Published: April 2011

Abstract
The location of labelled probucol in lipoprotein particles was investigated in-vitro. Human serum was incubated for 4 h at 37°C with [14C]probucol to incorporate probucol into lipoproteins. Serum lipoprotein particles were then isolated according to their apolipoprotein markers by sequential immunoaffinity chromatography at 4°C, and probucol concentration was determined in each lipoprotein fraction. Analysis of probucol distribution vs lipoprotein components revealed that probucol in particles strongly correlated with phospholipid concentration. Analysis of probucol distribution vs lipoprotein physical characteristics showed that probucol strongly correlated with the surface area of the monolayer surrounding the lipidic core of particles constituting phospholipids and free cholesterol. These data support the hypothesis that probucol is preferentially located in the phospholipid/free cholesterol monolayer surrounding the lipid core, in the vicinity of cholesteryl ester at the core surface or in the vicinity of hydrophobic areas of apolipoprotein that faces the monolayer.
Inhibition of Monoamine Oxidase from Bovine Retina by β-Carbolines
Authors: De Arribam A. Fernández , Lizcano J M , Balsa M D , Unzeta M 
Published: April 2011

Abstract
The behaviour of some β-carboline derivatives as inhibitors of monoamine oxidase has been studied in bovine retina. Inhibition was found not to show any significant time dependence. Di- and tetrahydro-β-carbolines were shown to behave as reversible and competitive inhibitors. In contrast, the fully unsaturated β-carbolines harmane, harmine and harmaline, which showed deviation from linearity at high substrate concentrations, behaved as tight-binding inhibitors. In these cases, the concentration of the enzyme and the inhibitor were of the same order. This was confirmed by the Ki values for these compounds in the nanomolar concentration range. Consistent with this was that inhibition was only partly reversed by dialysis for 18 h at 4°C, although complete reversal was observed after dialysis for the same period at 37°C. Structure-activity relationships indicated that substitution of a methoxy group at the C7 position of the aromatic ring is determinant for this tight-binding behaviour; a substitution of this group at the C6 position greatly reduced inhibition. Since β-carbolines have been reported to be formed endogenously, this suggests that they might have important physiological actions on monoamine oxidase activity in-vivo. In contrast, all the β-carbolines investigated in this study had low potencies as inhibitors of monoamine oxidase B.
The Anticonvulsant FCE 26743 is a Selective and Short-acting MAO-B Inhibitor Devoid of Inducing Properties towards Cytochrome P450-dependent Testosterone Hydroxylation in Mice and Rats
Authors: Benedetti M Strolin , Marrari P , Colombo M , Castelli M G , Arand M , Oesch F , Dostert P 
Published: April 2011

Abstract
The effects of the potent anticonvulsant FCE 26743 ((S)-2-(4-(3-fluorobenzyloxy)benzylamino)propionamide) on monoamine oxidase (MAO) activity were measured in-vitro and ex-vivo using rat tissue homogenates. In-vitro, FCE 26743 showed potent and selective inhibitory properties towards liver MAO-B, with IC50 values about 10−7 m for MAO-B and higher than 10−5 m for MAO-A. When determined ex-vivo in brain, the ED50 value for the inhibition of MAO-B was 1·1 mg kg−1 (p.o.) 1 h post-dosing, whereas MAO-A remained virtually unaffected after administration of 60 mg kg−1. Similar effects were seen in liver. Following oral administration of 5 mg kg−1 FCE 26743 to rats, brain MAO-B inhibition was 79% after 1 h and 13% after 24 h, indicating that FCE 26743 behaves as a short-acting MAO-B inhibitor. The ability of FCE 26743 to act as a MAO substrate was assessed in mice by measuring the urinary excretion of alaninamide, a potential metabolite of FCE 26743 which would result from the action of MAO. No alaninamide was detectable in the 0–8 h urines after administration of a 119 mg kg−1 dose, suggesting that FCE 26743 is not, or only to a small degree, a substrate of MAO. The effects of FCE 26743 on cytochrome P450 enzymes involved in testosterone hydroxylation were determined in rats after repeated administration. No induction of the cytochrome P450 system was noted.
The Effect of Indobufen on the Activities of Selected Rat Liver Phase I and Phase II Drug Metabolizing Enzymes, Peroxisomal β-oxidation and Hepatic Glutathione Status
Authors: Thomas H , Benedetti M Strolin , Dostert P , Oesch F 
Published: April 2011

Abstract
Oral administration of indobufen to male rats for three days at daily doses of 5, 10 and 20 mg kg−1 resulted in no changes in liver total glutathione, cytosolic glutathione S-transferases or microsomal epoxide hydrolase. Reduced glutathione appeared slightly diminished to about 84% of control at the highest dose level. Microsomal cytochrome P450-dependent ethoxyresorufin O-de-ethylase and pentoxyresorufin de-alkylase activities were decreased to 64% (not significantly) and 67% of control at the lowest dose level. 6α- and 7α-Hydroxytestosterone activities were decreased to 67 and 68% of control at the highest dose level. Cyanide-insensitive peroxisomal fatty acid β-oxidation was increased to 223, 261 and 232% of control at doses of 5, 10, and 20 mg kg−1, respectively. The results obtained in this study are indicative of the action of indobufen as a weak peroxisome proliferator in male rat liver, and suggest a slight but toxicologically insignificant inhibitory action of this drug on microsomal cytochrome P450-dependent enzyme activities.
The effect of pectin on the gastric emptying rates and blood glucose levels after a test meal
Authors: Iftikhar S Y , Washington N , Wilson C G , MacDonald I A , Homer-Ward M D 
Published: April 2011

Abstract
This study was designed to evaluate the effect of pectin given in a palatable form on the gastric emptying rates of the solid and liquid phases of a test meal and to ascertain whether pectin affected blood glucose levels in ten healthy male and female volunteers. Gastric emptying was measured using dual isotope gamma scintigraphy. Allocation to the treatment group was double-blind and randomized. Sequential blood sampling was used to measure blood glucose levels. The times for the stomach to empty half the radiolabelled meal were similar after both pectin and placebo; however, a significant difference was seen between the AUC values of the meal between the two treatments. This can be attributed to the divergence of the emptying curves after the time point at which 50% of the meal had emptied, as pectin delayed the emptying of the last 20% of the meal. The initial phase of emptying for both pectin and placebo was significantly faster than the meal. No significant difference was found between blood glucose levels when either pectin or placebo was administered.
A Shape Factor to Characterize The Quality of Spheroids
Authors: Podczeck Fridrun , Newton John Michael 
Published: April 2011

Abstract
A shape factor eR has been devised to describe how the form of spherical particles approaches that of a true spheroid, based on a two-dimensional image analysis. Both the deviation of shape from a circle towards an ellipse and surface irregularities influence the value of eR. Using a set of model figures such as squares, triangles, diamonds and stars, it could be shown that eR clearly differentiates between different polygonally symmetric figures, even in the case where common shape descriptors such as the aspect ratio provide equal values. The value of eR is 1·0 in the case of a perfect spheroid, while ellipticity and surface roughness lead to a significant change in the value.
Ulcer-protecting Effects of Naringenin on Gastric Lesions Induced by Ethanol in Rat: Role of Endogenous Prostaglandins
Authors: Motilva V , De La Lastra C Alarcón , Martín M J 
Published: April 2011

Abstract
This study was designed to determine the cytoprotective properties of naringenin and the involvement of endogenous prostaglandins on mucosal injury produced by absolute ethanol. Gastric glands were also histologically analysed. Oral pretreatment with the highest dose of naringenin (200 mg kg−1), 240 min before absolute ethanol, was the most effective in ulcer prevention. Subcutaneous administration of indomethacin (10 mg kg−1) to the animals treated with naringenin (200 mg kg−1) partially inhibited the gastric protection but there was no increase in prostaglandin E2. All treated groups showed a marked increase in gastric mucus, although this increase was less in animals pretreated with indomethacin. Total proteins and hexosamine content decreased in the groups receiving indomethacin. Histomorphometric evaluation of the gastric damage, with the highest dose of naringenin (200 mg kg−1), confirmed a significant increase of mucus production accompanied by a parallel reduction of gastric lesion.
Effects of β-Adrenoceptor Antagonists on Portal Vein Hypertension and Ethanol-induced Gastric Mucosal Damage in Rats
Authors: Woo Patrick Chiu Yat , Cho Chi Hin 
Published: April 2011

Abstract
The effects of various β-adrenoceptor antagonists, with different pharmacological properties, on systemic and portal vein blood pressure and on ethanol-induced gastric mucosal damage were examined in surgically-induced portal hypertensive rats. Propranolol (5, 10 or 20 mg kg−1), nadolol (5 or 10 mg kg−1), metoprolol (10 or 20 mg kg−1), labetalol (20 or 40 mg kg−1) and pindolol (3 or 6 mg kg−1) reduced systemic blood pressure to a similar degree in both portal vein-ligated and sham-operated rats. All β-adrenoceptor antagonists, except for pindolol, significantly reduced portal venous pressure and ethanol-induced macroscopic gastric mucosal damage in portal hypertensive animals. Sham-operated rats had lower portal venous pressure and less gastric damage compared with portal hypertensive rats, but both were unaffected by β-adrenoceptor antagonist pretreatment. We conclude that: propranolol, nadolol, metoprolol and labetalol are effective in reducing the portal venous pressure and ethanol-induced gastric mucosal damage in portal hypertensive rats, but not in portal normotensive animals; there was no direct relationship between the reduction of portal vein and systemic blood pressure; and local anaesthetic action is probably important in reducing the portal vein pressure and ethanol-induced gastric mucosal lesions, while the intrinsic sympathomimetic effect can counteract the actions of the β-adrenoceptor antagonists on portal venous pressure and gastric mucosa.
Studies on the Mechanism of Spasmolytic Activity of (O-Methyl-)-N-(2,6-dihydroxybenzoyl)tyramine, a Constituent of Aniba riparia (Nees) Mez. (Lauraceae), in Rat Uterus, Rabbit Aorta and Guinea-pig Alveolar Leucocytes
Authors: Thomas George , Branco U J V Castelo , Filho J M Barbosa , Bachelet M , Vargaftig B B 
Published: April 2011

Abstract
The mechanism of action of a nonspecific smooth muscle relaxant, (O-methyl-)-N-(2,6-dihydroxybenzoyl)tyramine (riparin), a constituent of Aniba riparia (Nees) Mez. (Lauraceae) was studied in relation to Ca2+ metabolism in smooth muscle tissues and in guinea-pig alveolar leucocytes. In rat depolarized uterus, riparin inhibited in a reversible and noncompetitive manner CaCl2-induced contraction, a response mediated through voltage-dependent Ca2+ channels. The pD2 value (mean±s.e.m.) for riparin was 4·98±006. When compared with sodium nitroprusside (IC50 2·5 μm), an antagonist of receptor-operated Ca2+ channels, riparin was ineffective in suppressing noradrenaline-induced sustained contractions of rabbit aortic strips. However, in the aorta, the compound inhibited intracellular calcium-dependent transient contractions of noradrenaline and riparin (IC50 10·1 μm), was approximately two and a half times more potent than procaine (IC50 25·5 μm), a known inhibitor. In guinea-pig alveolar leucocytes, riparin (IC50 3·2 μm), inhibited intracellular Ca2+ accumulation induced by the calcium ionophore A23187. The results suggest that the inhibition of Ca2+ influx and of Ca2+ release from intracellular stores contribute to the spasmolytic effects of riparin, which may not involve cyclic AMP generation as the levels of this nucleotide were not increased in alveolar macrophages treated with riparin (10–100 μm).