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T Ceriani

Publications and source records attributed to T Ceriani.

At least 19 recordsLinked to original sources
PubMed1990

[Differences in potential and content of the mucus in the stomach of the rat with avitaminosis A].

Vitamin A (vit. A) acts in the synthesis of glycoproteins and in cell surface phenomena of epithelia. Since the glycoproteins of gastric mucus and the integrity of gastric cell membranes are components of gastric barrier (GB), vit. A could play a role in GB. Five groups of rats were used: I) rats fed on vit. A deficient diet; II) rats pair-fed plus a daily oral dose of 45 micrograms vit. A; III) normal rats; IV) rats recovered from avitaminosis A (avit. A) after 20 days of daily oral dose of 300 micrograms vit. A; V) rats pair-fed plus a daily oral dose of 45 micrograms vit. A. We measured: 1) transparietal gastric potential difference (PD) in vivo (by means of agar-KCl electrodes); 2) mucus (by binding of Alcian blue): in gastric mucosa; adherent to gastric mucosa; in gastric lumen; 3) dry weight of the stomach. Avit. A induced: i) a decrease of PD and mucus in mucosa and lumen; ii) an increase of mucus adherent to mucosa; iii) an increase of the percentage of dry weight on wet weight. All parameters were normal after recovery from avit. A. Results suggest that avit. A could reduce either mucus synthesis or its erosion. Moreover avit. A might modify mucus structure and sterical configuration of mucosal cells. The alteration of mucosal cell membranes could decrease PD. In conclusion the modifications of some components of rat GB seem specifically caused by avit. A and suggest a protective role of vit. A.

Animals↗
PubMed1987

Circadian rhythmicity of acid secretion and electrical function in intact and injured rat gastric mucosa--the relation of timing to ulcerogenesis.

Alteration of electrical function in mammalian gastric mucosa is considered as an indicator of gastric barrier rupture. Measurements of transmucosal potential difference (PD) and electrical resistance (R) have documented such alterations to a variety of mucosal damaging agents. This study was designed to test whether the rat gastric mucosa exhibits circadian rhythms in acid secretion and electrical function and whether the damage produced by a mucosal acting agent (butyric acid) is also circadian-stage dependent. Mucosa was isolated from the gastric body of male rats standardized from birth to a light-dark regimen. Circadian rhythms of acid secretion and PD and R with acrophases during the dark hours were documented. Administration of butyric acid produced circadian-stage dependent damage with an acrophase also during the dark-phase span. Thus, in this experimental model, measurements of electrical function represented a poor index of gastric mucosal susceptibility to damaging agents. The authors discuss the possibility that rhythms other than those related to electrical function may better define mucosal vulnerability to ulcerogenesis.

Animals↗
PubMed1987

Circadian rhythms of acid secretion and electric parameters in rat gastric mucosa in vitro.

In male Wistar rats standardized from birth in LD 12:12 conditions (with light from 0700 to 1900 hr), samples of mucosa from the body of the stomach were isolated in vitro and mounted in a Ussing-type chamber. Spontaneous secretion of the hydrogen ion (H+)during 45 min of incubation was measured. Some electric parameters [transmucosal potential difference (PD) and electrical resistance (R)] were detected in the gastric mucosa both during H+ secretion and during inhibition of acid secretion by cimetidine. The variables studied were analyzed with the single cosinor method, and all revealed a circadian rhythm with acrophases during the dark span. The higher values of PD and R found during the dark hours are unrelated to acid secretion and may indicate a greater efficiency of ionic pumps and a limited passive permeability.

Animals↗
PubMed1984

Gastric mucosa permeability and HCO3- secretion 'in vivo' during perfusion of damaging and protective agents across canine Heidenhain pouches.

UNLABELLED: Gastric mucosal barrier of 'in vivo' dogs with a Heidenhain pouch (HP) was broken by butyric acid (BA). Cimetidine intravenously (5 mg/kg/h) prevented HCl secretion. Unidirectional fluxes of H+ and Na+, passive mucosal permeability [evaluated with a low-molecular-weight substance, polyethylenglycole 200(PEG 200)] were increased by BA while transparietal potential difference (PD) was depressed. HCO3- secretion, measured as PCO2 in HP, was incremented . Intragastric perfusion of acetazolamyde (Az) increased loss of BA from HP and enhanced the rupture of gastric mucosa. HCO3- secretion was depressed by Az. Intragastric perfusion of gastric phosphodiesterases inhibitors, theophylline (Th) and 3-isobutyl-1-methylxanthine (IMX), recovered the resistance of gastric mucosa both to ions and PEG 200. Nevertheless HCO3- secretion remained high. IN CONCLUSION: i) cytoprotection of gastric mucosa with either Th or IMX was effective to normalize its resistance to ions and low-molecular-weight substances; ii) increment of HCO3- secretion during cytoprotection was uncoupled with mechanisms dependent on membrane permeability.

1-Methyl-3-isobutylxanthine↗
PubMed1980

[Effect of the association of inhibitors of the H 1 and H 2 histamine receptors in the mechanism of rupture of the gastric barrier in the dog in vivo].

Two specific inhibitors of histamine receptors, H1 mepiramine (Mp) and H2 cimetidine (Cm), were used in combination to define the role of histamine in the mechanisms of gastric barrier rupture in the dog "in vivo". A gastrolesive substance butyric acid (Ac.B. 75 mM) in hydrocloric acid solution (HCl 75 mM) was perfused through Heidenhain pouches in the presence or absence of Mp (10 mg/Kg i.m.) and Cm (1 mg/Kg/h i.v.). The results obtained showed: 1) Ac.B. caused a remarkable increase in H+ and Na+ fluxes, enhanced K+ secretion and decreased transparietal potential difference (D.P.). 2) Histamine inhibitors in combination uneffected changes of the ionic fluxes and D.P. produced by Ac.B. 3) Reversal to normal of both ionic fluxes and D.P. was not accelerated by the combination of Mp and Cm. The conclusion was reached that in the initial phase of gastric barrier rupture damage of gastric mucosa occurs by mechanisms non histamine-dependent.

Animals↗
PubMed1980

[Electroneutrality of the gastric fluids in the dog in vivo with Heidenhain denervated gastric pouches].

Ionic fluxes and electroneutrality were studied during HCl and fatty acids perfusion through canine Heidenhain pouches. Fatty acids at low concentrations were incapable of modifying the percentages of ionic movements observed during HCl perfusion. In spite fatty acids induced modest signs of gastric mucosal injury like increased disappearance of H+, increased appearance of Na+ in the contents, reduction in potential difference. Results obtained either in the presence or absence of fatty acids showed: 1. at low HCl concentration exchange-diffusion of Na+ for H+ occurred at 1:1 mole basis; 2. at high HCl concentrations increased movement of H+ to blood and decreased movement of Na+ to gastric contents caused a greater diffusion of Cl- out of pouches.

Animals↗
PubMed1978

Kinetics of D-histidine diffusion across rat intestine in vitro.

A five-compartment linear model for diffusion in vitro across rat jejunum has been proposed for the study of the kinetic constants of D-histidine transport. Once preliminary experiments using 2,4-dinitrophenol and L-methionine have proved that D-histidine gives rise to passive transport only, the validity of the model was tested and its parameters estimated through a best-fitting procedure by using experimental data concerning D-histidine transport. D-Histidine diffusion was studied in everted and unreverted loops mounted in an oxygenated bath system. Both mucosa to serosa and seroa to mucosa movements of D-histidine (3-30 mM) were evaluated by measuring chemically the amount of D-histidine transported into intestinal lumen every 5 min for 60 min. Results obtained proved that D-histidine transport in each direction (mucosa to seroa or seroa to mucosa) was dependent-concentration process. Nevertheless different values of gain and time constants were estimated for the transport in the two directions.

Animals↗
PubMed1976

Numerical determination of intestinal membrane diffusing constants by a gradient method.

Optimisation problems arising in the identification of kinetic parameters of intestinal membranes are here considered. The dynamic behaviour of the membrane is described by means of a linear compartmental model. Using optimisation techniques of a gradient type, the intestinal kinetic parameters are identified, minimising a quadratic criterion between experimental data of D-histidine transport and model prediction. Numerical results are reported and their physiological implications discussed. The quantitative assessment of the asymmetry of diffusion constants with respect to diffusion direction seems to be an important result of this work.

Biological Transport↗