Search PubMed⌕ Search

Biomedical subjects

J Frexinos

Publications and source records attributed to J Frexinos.

At least 55 records · Page 3Linked to original sources
PubMed1994

Homologous desensitization of PAF receptors via a PGE2-dependent pathway on intestinal smooth muscle.

The aim of the present study was to evaluate the effect of in vitro preincubation with PAF of isolated smooth muscle cells from guinea pig ileum in order to assess possible PAF receptor desensitization. Cells dispersed by enzymatic digestion were preincubated with PAF for 30 min and the contractile effect of PAF was then assayed. In cells preincubated for 30 min with 10 nM PAF, the concentration inducing maximal cell contraction was 1 microM instead of 10 nM in freshly dispersed cells and the EC50 was 40 nM instead of 10 pM. This desensitization to the contractile effect of PAF was prevented when cells were preincubated for 30 min with PAF plus PAF antagonist BN52021, PGE2 antagonist SC19220, cyclooxygenase inhibitor indomethacin and the phospholipase A2 inhibitor bromophenacyl bromide. In similar experiments, no desensitization occurred for CCK8 receptors after preincubation with either PAF, PGE2 or CCK8. These results indicate that homologous desensitization of PAF receptors could occur via a PGE2-dependent pathway in intestinal smooth muscle cells from guinea pig.

Acetophenones↗
PubMed1993

Stimulatory (EP1 and EP3) and inhibitory (EP2) prostaglandin E2 receptors in isolated ileal smooth muscle cells.

Isolated smooth muscle cells from the circular layer of pig and guinea-pig ileum were used to study the effect of prostaglandin E2 (PGE2) and three PGE2 receptor (EP) agonists; iloprost (EP1), butaprost (EP2) and enprostil (EP3). In pig cells, PGE2 and enprostil induced cell contraction (22.1 and 21.5% shortening of cell length, obtained at 10 nM for PGE2 and 1 nM for enprostil, respectively). Iloprost and butaprost had no contractile effect. However, the cholecystokinin octapeptide (CCK-8; 10 nM)-induced contraction was inhibited when cells were preincubated with iloprost or butaprost. In guinea-pig cells, PGE2, butaprost and iloprost induced cell contraction, whereas enprostil had no effect (23.1% for 10 nM PGE2, 22.8% for 1 nM butaprost and 22.6% for 10 nM iloprost). Preincubation with SC19220 (EP1 antagonist) inhibited the PGE2-, butaprost- and iloprost-induced contractions. When the contractile effect of PGE2, butaprost and iloprost was inhibited by addition of SC19220, these agents inhibited the cell contraction induced by CCK-8 (1 nM). Smooth muscle cells from guinea-pig and pig ileum express two PGE2 receptor subtypes that induce opposite effect. EP1 and EP3 receptors mediate cell contraction in guinea-pig and pig, respectively, whereas EP2 receptors mediate cell relaxation in both species.

Alprostadil↗
PubMed1993

Platelet-activating factor (PAF) induces a contraction of isolated smooth muscle cells from guinea pig ileum: intracellular pathway involved.

This study was designed to evaluate the effect of platelet-activating factor (PAF) on isolated smooth muscle cells from guinea pig ileum circular layer, to characterize the PAF receptors involved in this effect and to determine the intracellular pathways triggered by PAF. Cells dispersed by enzymatic digestion were incubated for 30 sec in the presence of PAF and fixed by glutaraldehyde. When inhibitors or antagonists were tested, cells were preincubated with them for 1 min. Then PAF was added for 30 sec, and the cells were fixed. Contraction was assessed by measuring the length of 50 cells and was expressed as the percentage decrease in cell length from controls. The relaxing effect of inhibitors was expressed as the percentage of the maximal contraction observed in their absence. PAF induced a cell contraction in a concentration-dependent manner. Maximal contraction (24.2 +/- 4.2%) was obtained for a PAF concentration of 10 nM (EC50 = 10 pM). PAF-induced contraction was inhibited by the PAF receptor antagonists BN52021, L659.989 and SR27417. Contraction induced by 10 nM PAF was inhibited when cells were incubated in Ca(++)-free medium with or without 2 mM EGTA or in a 1 mM Ca++ medium to which 100 nM nifedipine was added. When cells were preincubated with concentrations ranging from 0.01 pM to 10 microM of relaxing agents (vasoactive intestinal polypeptide, forskolin, 8 Bromo cAMP) known to increase the intracellular level of cAMP, PAF-induced contraction was inhibited. Moreover, when cells were preincubated with pertussis toxin (200 ng/ml) or cholera toxin (8.4 ng/ml), contraction induced by PAF was also inhibited.(ABSTRACT TRUNCATED AT 250 WORDS)

8-Bromo Cyclic Adenosine Monophosphate↗
PubMed1992

Differences between jejunal myoelectric activity after a meal and during phase 2 of migrating motor complexes in healthy humans.

Using an intraluminal probe with six pairs of annular electrodes, the myoelectric activity of the proximal jejunum was recorded during 48-hr sessions in 16 healthy volunteers receiving evening and noon meals (1000 kcal) and breakfast (400 kcal). In 10 subjects receiving no drug, the characteristics of the migrating motor complexes (period, duration of each phase, velocity of propagation of phase 3, duration of the postprandial disruption) varied markedly between subjects but were relatively constant from the first to the second day of recording. Single spike bursts propagated at a rate of 2-5 cm/sec, clusters of 3-10 spike bursts propagated at a rate of 0.5-1 cm/sec, and similar clusters recurring repetitively each 1.5-2 min were observed after the meals and very rarely in the fasted state during phase 2 of nocturnal migrating motor complexes. In six subjects, oral administration of codeine (50 mg) 1 hr before a meal induced migrating motor complexes in the postprandial state, with characteristics similar to that observed in the fasted state except a longer duration of phase 2. Single spike bursts and isolated and repetitive clusters of spike bursts were observed during phase 2 of the codeine-induced migrating motor complexes and after meals preceded by placebo, but very rarely during the phase 2 of nocturnal (fasted state) migrating motor complexes. It is concluded that the patterns of jejunal contractions consisting of propagated single spike bursts and isolated or repetitive spike bursts characterize the postprandial state in healthy humans and are dependent upon digesta flow.

Adult↗
PubMed1992

Microscopic examination of bile directly collected during endoscopic cannulation of the papilla. Utility in patients with suspected microlithiasis.

The usefulness of microscopic examination of pure bile directly collected from the biliary tract during endoscopic retrograde cholangiography and without hormonal simulation was prospectively evaluated in 72 patients. According to clinical, biochemical, ultrasonographic, and radiographic data, the patients were separated into two groups: group 1, patients with proven stones (N = 50), and group 2, patients with suspected microlithiasis presenting symptoms suggestive of cholelithiasis but without evidence of macroscopic stones at echography or cholangiography (N = 22). Cholesterol crystals and/or bilirubinate granules were observed (eg, positive examination) in the bile of 41 of the 50 patients of group 1 (82%). Among patients of group 2, seven (32%) had a positive bile examination: cholecystectomy (N = 2) or endoscopic sphincterotomy (N = 5) disclosed minute stones in all cases. In the 15 patients of group 2 with a negative bile examination, cholecystectomy (N = 3), sphincterotomy (N = 2), and clinical (and/or echographic) 20-month follow-up (N = 9) revealed biliary lithiasis in only one patient, in whom recurrent cholangitis led to disclosure of one bile duct stone. According to these results, microscopic examination of bile samples collected during endoscopic retrograde cholangiography exhibited a sensitivity and a specificity for cholelithiasis recognition of 82.7% and 100%, respectively, with a positive predictive value of 88%. We conclude that the accuracy of this method makes it useful to investigate and manage patients with suspected microlithiasis.

Aged↗
PubMed1992

Cholecystokinin and gastrin induce cell contraction in pig ileum by interacting with different receptor subtypes.

The aim of this study was to determine the cholecystokinin (CCK) receptor subtype involved in the direct myogenic effect of CCK on pig ileum. Smooth muscle cells were dispersed from pig ileum circular muscle layer and incubated in the presence of various concentrations of CCK agonists and antagonists. Contraction was assessed by measuring the length of 50 cells and expressed as the percentage decrease in cell length from control. Maximal contraction varied between 19% +/- 3% (gastrin II, 10 nmol/L) and 26% +/- 3% [CCK octapeptide (CCK-8), 10 nmol/L]. EC50 for CCK tetrapeptide (CCK-4) was the same than for pentagastrin (30 pmol/L), which were more potent than CCK-8 (100 pmol/L) and unsulfated gastrin 17 (100 pmol/L), which in turn were more potent than unsulfated CCK heptapeptide (CCK-7; 300 pmol/L) and sulfated gastrin II (300 pmol/L). The maximal contraction induced by synthetic analogs of CCK was 22% +/- 1% for 1 nmol/L JMV 170 and 23% +/- 1% for 10 nmol/L JMV 180. EC50 was 10 pmol/L for JMV 170 and 800 pmol/L for JMV 180. Contraction induced by 10 nmol/L CCK was inhibited as follows: L 365,260 half maximal inhibition (IC50) = 1 nmol/L greater than L 364,718 (IC50 = 90 nmol/L) greater than proglumide (IC50 = 1 mumol/L). Contraction induced by 10 nmol/L unsulfated gastrin 17 was inhibited as follows: L 365,260 (IC50 = 1 pmol/L) greater than L 364,718 (IC50 = 60 nmol/L) greater than proglumide (IC50 = 4 mumol/L). Removal of Ca2+ from the extracellular medium did not alter the contraction induced by CCK-8 (10 nmol/L) but impaired the contraction induced by unsulfated gastrin 17 (10 nmol/L) -56% in Ca(2+)-free medium, -77% in Ca(2+)-free medium plus 2 mmol/L EGTA, and -70% in the presence of 1 mumol/L nifedipine. These results show that the CCK receptor of pig ileum smooth muscle cells is closely similar to the B receptor and is not dependent on an influx of extracellular Ca2+ to induce cell contraction. By contrast, gastrin could act through a specific receptor subtype, the "gastrin receptor," triggering a Ca2+ influx into the cell to induce cell contraction.

Animals↗
PubMed1992

Comparative effects of galanin on isolated smooth muscle cells from ileum in five mammalian species.

Effect of galanin and CCK8 were studied on isolated smooth muscle cells obtained from pig, guinea-pig, rat, rabbit and dog ileum circular muscle layer. Galanin as well as CCK8 induced a concentration-dependent contraction of pig, rat, rabbit and guinea-pig ileum smooth muscle cells. Maximal contraction ranged between 23.7 +/- 1.9% and 26.1 +/- 3.1% decrease in cell length from control in the presence of both peptides. This maximal contraction was obtained at 1 nM galanin in pig, rat, rabbit, 1 nM CCK8 in rat, rabbit, guinea-pig, at 10 nM galanin in guinea-pig and 10 nM CCK8 in pig. Concentrations of galanin inducing a half maximal contraction (EC50) ranged between 8 pM and 80 pM in these species. In dog, CCK8 induced a concentration-dependent contraction of ileum smooth muscle cells, with a maximal contraction (24.5 +/- 2.3%) at 1nM and an EC50 of 50 pM while galanin inhibited cell contraction induced by CCK8. The CCK-induced contraction was abolished at 10 nM galanin and 10 nM VIP. Concentrations of galanin and VIP inducing a half-maximal relaxation of contracted cells were 2 pM and 3 pM respectively. It is concluded that galanin may induce cell contraction of pig, guinea-pig, rat and rabbit ileum circular muscle layer and cell relaxation of dog ileum by a direct myogenic effect.

Animals↗
PubMed1992

Intracellular pathways triggered by galanin to induce contraction of pig ileum smooth muscle cells.

1. In order to determine the intracellular mechanisms by which galanin induces contraction of isolated smooth muscle cells from pig ileum, we examined the effects of external Ca2+, relaxing agents, pertussis toxin and forskolin on the galanin-induced contraction and compared these effects to those observed on the cholecystokinin derivative CCK8-induced contraction. 2. Galanin induced a concentration-dependent cell contraction. The maximal contraction (24.5 +/- 2.1% of the length of resting cells) was observed at 1 nM of galanin. When cells were incubated in the simultaneous presence of concentrations of galanin (10 fM) and CCK8 (1 pM) which were ineffective alone, or galanin (10 fM) and acetylcholine (100 pM), a synergistic action was observed corresponding to a submaximal contraction. 3. Incubation of cells in Ca(2+)-free medium caused a significant decrease in galanin- but not in CCK-induced contraction. Nifedipine, a Ca2+ channel blocker, provoked a concentration-dependent inhibition of galanin-induced contraction while it had no effect on the contraction induced by CCK8. 4. Vasoactive intestinal polypeptide (VIP) and isoprenaline, known to induce cell relaxation through an increase in intracellular cAMP level, inhibited CCK-induced cell contraction at concentrations ranging from 1 pM to 1 microM but failed to inhibit cell contraction induced by galanin. 5. When cells were pre-incubated for 3 h in the presence of 200 ng/ml of pertussis toxin, the contraction induced by galanin was abolished while the CCK-induced contraction remained unchanged. On the contrary, 10 microM forskolin abolished the contraction induced by 10 nM CCK but had no effect on galanin-induced contraction. 6. These results indicate that galanin induces a concentration-dependent contraction of pig ileum smooth muscle by a direct myogenic effect. This effect of galanin involves the activation of a pertussis toxin-sensitive G protein, which results in an influx of Ca2+ into the cell. This intracellular pathway is insensitive to the relaxing effect of cAMP.

Acetylcholine↗
PubMed1992

[Incidence, treatment and prognosis of cancer of the pancreas in Haute-Garonne (1982-1986)].

The characteristics of incident cases of pancreatic carcinoma found in the area of Haute-Garonne (France), as determined by the Digestive Cancer Registry, are reported. Two hundred and forty-six new cases were collected during a 5 year period in a population of 820,000 inhabitants. The annual standardized incidence rate per 100,000 inhabitants was 4.7 for men and 2.6 for women, respectively. This represents a low risk and corresponds to 7 percent of all intestinal tract tumors. The tumors were shown histologically to be adenocarcinoma in 85 percent of cases. The tumor was localized in the head of the gland in 64 percent of cases, while metastases were present at the time of diagnosis in 43 percent of cases. Ultrasonography was the initial investigation (44 percent of cases) and was performed well before endoscopic retrograde wirsungography (12.8 percent) and computed tomography (18 percent). Eighty-six percent of the patients were operated on. Curative surgery, however, was possible in only 12.5 percent of patients. The incidence of carcinoma remained stable during the observation period and no change was noticed with regard to housing conditions. During follow-up, 50 of 215 patients died within one month following the diagnosis (23 percent). Actuarial survival was 36 percent at 6 months, 17.4 percent at one year, and 3.6 percent at 3 years. These data were comparable to those observed in the Côte-d'Or and Calvados areas. These findings suggest that the French Digestive Tumor Registries should develop co-operative studies particularly in the analytic epidemiological fields.

Actuarial Analysis↗
PubMed1991

Galanin induces contraction of isolated cells from circular muscle layer of pig ileum.

The effects of galanin and its interaction with cholecystokinin and acetylcholine on smooth muscle cells were studied in vitro on isolated cells obtained from pig ileum circular muscle layer. Galanin induced a concentration-dependent cell contraction with a maximal contraction (24.5% decrease in cell length from control) obtained at 1 nM. The concentration of galanin inducing a half-maximal contraction was 3 pM. Tetrodotoxin (10 microM) failed to inhibit cell contraction induced by galanin (1 nM), pentagastrin (10 nM) and acetylcholine (1 microM). Atropine abolished the contraction induced by acetylcholine (1 microM), but had no effect on galanin- and pentagastrin-induced contraction. L 364,718 inhibited the contraction induced by CCK8 but not the galanin-induced contraction. At the uneffective concentration of 10 fM, galanin had a synergistic effect with an uneffective concentration of CCK8 (1 pM). These results suggest that (i) galanin contracts smooth muscle cells from pig ileum by acting on a specific receptor; (ii) galanin and either CCK or acetylcholine may act in a synergistic way to induce cell contraction.

Acetylcholine↗
PubMed1991

[Acute recurrent colonic pseudo-obstruction. Report of a case occurring during and following pregnancy and treated by total colectomy].

The authors report a case of multi-recurrent Ogilvie's syndrome during pregnancy, the post-partum period and a long time after deliver. Electromyographic and manometric studies excluded colonic inertia and disseminated gastrointestinal involvement. Total colectomy was performed after the 6th recurrence, resulting in complete cure of the patient.

Acute Disease↗
PubMed1990

Oral prostaglandin E analogues induce intestinal migrating motor complexes after a meal in dogs. Evidence for a central mechanism.

The effects of oral, intravenous, and intracerebroventricular administration of synthetic derivatives of prostaglandins E1 (misoprostol) and E2 (enprostil) on postprandial gastrointestinal motility were investigated in dogs chronically fitted with strain gauge transducers on the antrum and the proximal and middle jejunum. Synthetic prostaglandin E analogues administered orally at a dose of 20-50 micrograms/kg 15 min before the meal did not modify the postprandial pattern of gastric contractions but suppressed the spontaneous postprandial irregular activity on the jejunum and induced a cyclic pattern of migrating motor complexes for 4-6 h after the meal. These postprandial migrating motor complexes induced by prostaglandin E were propagated between the two recording sites and had a period similar to that observed in the fasted state. However, the duration of phase 2 was significantly increased and the amplitude of the phase 3 decreased. This jejunal cyclic motor pattern was reproduced by administration of synthetic prostaglandin E derivatives either intravenously (4-10 micrograms/kg) 15 min before the meal or intracerebroventricularly (50 ng/kg) 1 h after the meal. The intestinal migrating motor complex activity observed after oral administration of synthetic prostaglandin E derivatives was abolished by the previous intracerebroventricular (40 micrograms/kg) but not intravenous (200 micrograms/kg) administration of SC-19220, a receptor antagonist of prostaglandin E. These results suggest that oral administration of synthetic prostaglandin E1 (misoprostol) or prostaglandin E2 (enprostil) analogues before a meal induces postprandial migrating motor complexes on the jejunum in dogs through a mechanism involving central prostaglandin receptors.

Administration, Oral↗