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Biomedical subjects

G Soldani

Publications and source records attributed to G Soldani.

At least 55 records · Page 3Linked to original sources
PubMed1991

Cholinergic neurons and muscarinic receptors regulate anion secretion in pig distal jejunum.

The neurotransmitter acetylcholine is thought to modulate epithelial ion transport in the mammalian small intestine. In this study, the non-selective acetylcholine agonist, carbachol, produced rapid changes in short-circuit current (Isc), an electrical measure of active anion secretion, across isolated sheets of the distal jejunal mucosa-submucosa from swine. The potency of carbachol in elevating Isc was decreased 26-fold in the presence of 10 nM atropine, but remained unchanged by 1-100 microM hexamethonium or 0.1 microM tetrodotoxin. The acetylcholine antagonists produced little or no decrease in spontaneous Isc, whereas tetrodotoxin decreased Isc by 54 microA/cm2. [3H]Quinuclidinyl benzilate (QNB), a muscarinic acetylcholine receptor blocker, bound to a single species of sites within the mucosa-submucosa with a KD = 38 pM and Bmax = 94 fmol/mg protein. Selective muscarinic acetylcholine receptor blockers competed with [3H]QNB for this site with a rank order of affinity indicative of an interaction with a M3-muscarinic acetylcholine receptor. Specific [3H]QNB binding sites were autoradiographically localized in the jejunal wall to the epithelium, submucosa and muscularis propria. Transmural electrical stimulation (3-600 pulses/10 s, 0.5 ms, 60 V) of the mucosa-submucosa produced increases in Isc which were dependent upon the number of impulses delivered and did not undergo tachyphylaxis upon repeated stimulation. Responses to electrical transmural stimulation were inhibited by atropine and hexamethonium, as well as the respective neuronal Na+ and Ca2+ channel blockers tetrodotoxin and omega-conotoxin GVIA, suggesting that electrical transmural stimulation depolarizes submucosal cholinergic neurons which terminate on ion-transporting epithelial cells.(ABSTRACT TRUNCATED AT 250 WORDS)

Acetylcholine↗
PubMed1991

Development of small-diameter vascular prostheses which release bioactive agents.

A porous, distensible, tubular membrane which incorporates albumin and basic Fibroblast Growth Factor (bFGF), and is potentially utilizable as a bioactive small-diameter vascular prosthesis, was fabricated by a combined spraying, phase-inversion technique using a suspension of albumin and bFGF into a polyetherurethane-urea (Biomer) solution in dimethylacetamide (DMA). Scanning electron microscopy showed a material with an open-cell trabecular structure and small particles of albumin and/or bFGF entrapped in the bulk of the polyurethane trabeculae. The material released albumin and bFGF at an approximately constant rate for at least 2 weeks. The bFGF initially incorporated in the polymer remained biologically active as shown by in-vitro proliferation of human endothelial cells.

Albumins↗
PubMed1991

Bioartificial polymeric materials obtained from blends of synthetic polymers with fibrin and collagen.

A new class of biomaterials, called "bioartificial polymeric materials", was prepared blending a segmented polyurethane (PU) with fibrinogen (FBNG); and poly(acrylic acid) (PAA), poly(acrylamide) (PAAM), poly(vinyl alcohol) (PVAL), with collagen (CLG), respectively. The PU-FBNG material was processed through a spraying, phase-inversion technique to fabricate porous tubular conduits. FBNG was subsequently converted into covalently cross-linked fibrin (FBN) through the action of thrombin (Th), fibrin-stabilizing factor (FSF), and calcium ions. Differential scanning calorimetry (DSC) showed the cross-linked blend was more stable than native cross-linked FBN. Tensile behaviors of the PU-FBN materials closely matched those of a natural artery on varying the ratio PU/FBN. Implantation experiments in the rat model showed a mature internal capsule and good tissue organization of PU-FBN (50%) grafts in the regenerated arterial wall. However, 50% of FBN did not assure adequate mechanical resistance, and aneurysmal changes were seen in some grafts. DSC of CLG-based materials, processed by casting, showed that the synthetic component offered definite advantage compared to the CLG denaturation temperature, particularly noticeable for CLG-PAA and CLG-PVAL blends. Material advantages and drawbacks are discussed.

Animals↗
PubMed1990

Molecular design, synthesis, and antiinflammatory activity of a series of beta-aminoxypropionic acids.

Previous experimental and theoretical studies carried out on the mechanism of action of adrenergic drugs have shown that the (methyleneaminoxy)methyl moiety (C = NOCH2, MAOMM) can be considered as a "bioisostere" of an aryl group (Ar). On this basis, a series of substituted beta-aminoxypropionic acids (AOPAs) were synthesized as analogues of antiinflammatory arylacetic acids (ArAAs), in which the Ar portion is substituted by the MAOMM, with the aim of evaluating whether any antiinflammatory activity could be obtained from this class of drugs after the substitution of the Ar with the MAOMM. The antiinflammatory activity of the AOPAs synthesized was determined by carageenan-induced rat paw edema, using diclofenac as the reference drug. The pharmacological data showed that most of the AOPAs examined exhibit a significant antiinflammatory activity, which in the case of the (E)-3-(benzylideneaminoxy)propionic acid (7q) is very close to that of the reference drug. Structural and theoretical studies were carried out in order to compare the conformation and the molecular reactivity of the AOPAs with those of the ArAAs. Pharmacological results showed that the ArAAs also generally exhibit an antiinflammatory activity after the substitution of the Ar with the MAOMM, thus supporting the hypothesis of a bioisosterelike relationship between these two moieties in this class of NSAIDs.

Alanine↗
PubMed1990

Short-term effects of diethylaminoethyl-dextran on postprandial gastrointestinal hormone responses in man.

The effects of oral diethylaminoethyl-dextran (3 g total), taken 30 min before a standard mixed test meal, on plasma glucose, total cholesterol, triglycerides, total lipids, gastrin-like immunoreactivity, bombesin-like immunoreactivity, gastric-inhibitory-polypeptide-like immunoreactivity and neurotensin-like immunoreactivity were evaluated in eight healthy volunteers following a double-blind protocol. Incremental peak plasma concentrations of total lipids and triglycerides were significantly reduced by pretreatment with diethylaminoethyl-dextran pretreatment, while peaks of plasma glucose and total cholesterol were not significantly affected. Diethylaminoethyl-dextran also inhibited postprandial gastrin-like gastric-inhibitory-polypeptide-like and neurotensin-like immunoreactivity; by contrast, bombesin-like immunoreactivity was not significantly modified. The present study indicates that diethylaminoethyl-dextran is able to regulate some postprandial metabolic and hormonal parameters in man; consequently it might be useful in the treatment of hyperlipoproteinaemia and obesity.

Adult↗
PubMed1988

An analysis of the effects of galanin on gastric acid secretion and plasma levels of gastrin in the dog.

The effects of galanin on gastric acid secretion and plasma levels of gastrin were studied in conscious dogs chronically fitted with gastric fistulas. Continuous i.v. infusion of galanin (2 micrograms.kg-1.h-1) for 2 h did not affect unstimulated total acid output or plasma levels of gastrin. In contrast, simultaneous i.v. infusion of galanin (1-2 micrograms.kg-1.h-1) inhibited the bombesin-stimulated output of acid whereas the effects of bombesin on gastrin output were not significantly modified. Galanin (2-4 micrograms.kg-1 i.v.) also depressed the secretory response to 2-deoxy-D-glucose without significantly affecting plasma gastrin levels. Galanin (2-4 micrograms.kg-1 i.v.) did not depress bethanechol-stimulated gastric acid output or inhibit histamine-stimulated gastric acid secretion. These findings indicate that glanin inhibits the bombesin- and 2-deoxy-D-glucose-stimulated secretion of gastric acid in conscious dogs by an action which is probably exerted at the level of the cholinergic nerve terminals.

Animals↗
PubMed1988

Comparison of the gastric antisecretory effects of ramixotidine dihydrochloride (CM 57755), a new H2 receptor antagonist, and cimetidine in dogs.

This paper compares the effects of ramixotidine dihydrochloride (CM 57755) with those of cimetidine on gastric acid secretion and gastrin release in conscious dogs chronically fitted with Heidenhain pouches and/or gastric fistulae. At equimolar doses, intravenous (i.v.) or intragastric (i.g.) CM 57755 caused similar inhibition of dimaprit- or pentagastrin-induced secretion than cimetidine. Acid secretion stimulated by a meat meal was significantly reduced by both CM 57755 and cimetidine. Neither CM 57755 (4.5 and 9 mumol/kg) nor cimetidine (4 mumol/kg) modified gastrin release, while cimetidine (8 mumol/kg) significantly increased it. Judging from these results, while CM 57755 appears to be an inhibitor of gastric acid secretion induced by different stimulants in dogs with potency comparable to cimetidine. The increase in plasma gastrin levels seen after cimetidine but not after CM 57755 suggests that cimetidine releases gastrin by a mechanism independent of H2 receptor antagonism.

Animals↗
PubMed1987

The effects of the antimuscarinic drugs pirenzepine and atropine on plasma portal levels of somatostatin and gastrin in the dog.

The effects of the antimuscarinic drugs pirenzepine and atropine on somatostatin and gastrin portal levels under basal conditions and during bethanechol infusion have been investigated in anesthetized dogs. Iv bolus administration of pirenzepine (1 mg/kg) or atropine (0.1 mg/kg), decreased gastrin concentrations, but did not affect basal somatostatin levels. During 120 min of bethanechol infusion (160 micrograms/kg/h) gastrin levels increased but somatostatin levels were unchanged. Pirenzepine (1 mg/kg iv bolus), administered at the 60th min of bethanechol infusion, decreased the gastrin concentrations, and markedly enhanced somatostatin levels. Under the same conditions atropine (0.1 mg/kg iv bolus) decreased gastrin levels, but had little or no effect on somatostatin levels. These results indicate that muscarinic receptors with similar affinity for pirenzepine and atropine mediate excitatory cholinergic influences on gastrin release. By contrast, muscarinic receptors with higher affinity for pirenzepine seem to be involved in the cholinergic inhibition of somatostatin release: by selectively blocking these receptors, pirenzepine may increase portal somatostatin levels.

Animals↗
PubMed1987

Peripheral opioid receptors mediate gastrointestinal secretory and motor effects of dermorphin N-terminal tetrapeptide (NTT) in the dog.

Dermorphin N-terminal-tetrapeptide-amide (NTT) increased both basal and pentagastrin- or histamine-induced secretion in conscious dogs chronically implanted with both gastric fistulae and Heidenhain pouches. These excitatory effects were significantly prevented by the opioid receptor antagonists naloxone and N-methyl-levallorphan-methanesulphonate. In conscious dogs fitted with electrodes and strain-gauges in different parts of gastrointestinal tract, a premature phase III of the migrating myoelectric complex (MMC) in the duodeno-jejunum was triggered by NTT, while the activity of the antrum was not significantly modified. Further, the peptide enhanced the contractile activity of both proximal and distal portions of the colon, including a long-lasting period of increased muscle tone on the distal colon. Either naloxone or N-methyl-levallorphan-methanesulphonate completely prevented motor effects of NTT on gastrointestinal tract. It is concluded that NTT displays significant opiate-like activity on gastric acid secretion and intestinal motility of the dog by activating peripheral mu opioid receptors.

Animals↗
PubMed1987

The influence of a new prostaglandin E2 analogue (FCE 20700) on gastric acid and pepsin secretion in the dog.

The effects of FCE 20700, a new prostaglandin E2 analogue, on gastric acid and pepsin secretion stimulated by different secretagogues were studied in dogs. Intravenous FCE 20700 produced a significant inhibition of total acid output (TAO) induced by pentagastrin or histamine in gastric fistula (GF) dogs. This effect was short-lasting and mainly due to a reduction in the volume of gastric juice with little acid concentration change. TAO and pepsin output stimulated by 2-deoxy-D-glucose were similarly inhibited by intravenous FCE 20700. In dogs chronically fitted with both GF and Heidenhain pouch (HP), intragastric FCE 20700 significantly inhibited TAO stimulated by pentagastrin or histamine from HP, while acid secretion from GF was not significantly affected. It is concluded that FCE 20700 possesses a weak antisecretory activity in dogs. Consequently the antiulcer effects of this prostaglandin derivative seem to be largely independent from its influence on gastric acid and pepsin secretion.

Animals↗
PubMed1987

Effects of morphine on gastric ulceration, barrier mucus and acid secretion in pylorus-ligated rats.

The effects of intraperitoneal (IP) or intracerebroventricular (ICV) administration of morphine on acid and pepsin secretion, gastric ulceration and gastric bound mucoproteins were investigated in pylorus-ligated rats. Morphine, administered IP, produced a dose-dependent inhibition of the gastric secretion volume, acidity, pepsin output and bound mucoproteins. By contrast, the effect of morphine on gastric ulcers was not dose-dependent: a significant increase in gastric lesions was obtained with morphine 5 mg/kg IP. Naloxone IP prevented the effects of morphine on gastric secretory volume, acidity and pepsin output, but not on gastric mucus and ulcer score. ICV administration of morphine induced a dose-dependent inhibition of secretory volume, acidity and ulcer score, whereas no modification of gastric mucus was observed. Naloxone ICV prevented the effects of ICV morphine. Overall results suggest that morphine inhibits gastric secretion through both central and peripheral opioid receptors, whereas the inhibitory effect of morphine on bound mucus appears to be exerted on mucus synthesis through peripheral opioid receptors. This inhibitory effect on barrier mucus accounts at least in part for the gastric ulcerogenic action of morphine.

Animals↗
PubMed1987

Effects of white wine, Coke and water on basal and food-stimulated gastric acid secretion and gastrin release in the dog.

The effects of three types of white wine (10% ethanol; pH 2.84-3.26), Coke (pH 2.45) and water (pH 8.03) on basal and food-stimulated gastric acid secretion in dogs were investigated. Water and Coke did not significantly modify acid secretion and gastrin release under basal conditions. By contrast, white wine or water +10% ethanol significantly increased acid secretion, with a tendency to elevate plasma gastrin concentrations. Acid secretion and gastrin release induced by a standard meal were not significantly modified by previous administration of Coke and water. In contrast, white wine and water +10% ethanol significantly increased food-stimulated total acid output, without changing plasma gastrin levels. It is concluded that Coke and water have only trivial effects on basal and on food-stimulated gastric acid secretion and gastrin release in the dog. The gastric stimulant effect of white wine is mainly related to its percentage of alcohol regardless of the slight differences in pH of the solutions.

Animals↗
PubMed1986

Indirect stimulation by thyrotropin-releasing hormone of canine gallbladder motility.

Thyrotropin-releasing hormone (TRH) was unable to induce any noticeable contraction of canine isolated gallbladder strips up to the dose of 10(-4) g/ml, while caerulein (CAER) was spasmogenic in a dose-related manner beyond 10(-11) g/ml. This effect of CAER was unaffected by either atropine or tetrodotoxin. In conscious dogs, the intravenous bolus of TRH (20 micrograms/kg) or CAER (0.2-2.0 micrograms/kg) caused gallbladder emptying. The TRH response, unlike that of an equipotent dose of CAER, was prevented by atropine. In experiments on electrical activity of the digestive tract in conscious dogs, both TRH or CAER induced a concomitant increase on the myoelectrical activity in the proximal part of the small intestine. The excitatory effects were prevented by atropine only in the case of TRH. These results demonstrate that TRH stimulates indirectly the gallbladder and proximal duodenum of the dog. They suggest the involvement of a cholinergic pathway in this excitatory action.

Action Potentials↗