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Biomedical subjects

B Saffouri

Publications and source records attributed to B Saffouri.

15 recordsLinked to original sources
PubMed1988

Identical patterns of somatostatin secretion from isolated antrum and fundus of rat stomach.

The patterns of somatostatin secretion from the fundus, the main source of somatostatin, and the antrum, the site of paracrine regulation of gastrin secretion, were examined using perifused antral and fundic segments from rat stomach. Gastrin secretion fundic segments from rat stomach. Gastrin secretion could be obtained from antral segments only. Somatostatin secretion was obtained from both antral and fundic segments. 1,1-Dimethyl-4-phenylpiperazinium (DMPP) (10(-5) and 10(-4) M) and bombesin-14 (10(-8) and 10(-6) M) caused concentration-dependent increases in somatostatin secretion that were of the same magnitude in antral and fundic segments. These increases were also of the same magnitude as those obtained in the vascularly perfused whole stomach. Atropine (3 X 10(-7) M) inhibited the somatostatin response to DMPP (10(-4) M) to the same extent in antral (50 +/- 12% inhibition) and fundic (55 +/- 12% inhibition) segments. Hexamethonium (10(-5) M) also inhibited the response to DMPP to the same extent in antral (80 +/- 9%) and fundic (78 +/- 19%) segments. Methacholine caused a typically muscarinic decrease in somatostatin secretion that was of the same magnitude in antral (27 +/- 6%) and fundic (25 +/- 6%) segments. The identical patterns of somatostatin secretion from the two regions of the stomach imply that somatostatin secretion measured in the vascularly perfused whole stomach is a valid reflection of somatostatin secretion by the antrum.

Animals↗
PubMed1985

Healing of benign gastric ulcer. A placebo-controlled comparison of two dosage regimens of misoprostol, a synthetic analog of prostaglandin E1.

Misoprostol, a synthetic prostaglandin E1 methyl ester analog with gastric antisecretory and cytoprotective properties, prevents the development of acute experimental gastric and duodenal ulcers in various animal models. This study was designed as a multicenter randomized double-blind parallel-group comparison of the effects of two dosage strengths (25 and 100 micrograms q.i.d.) of orally-administered misoprostol and placebo on the healing of endoscopically-proven benign gastric ulcer in 299 out-patients. Safety was evaluated by comparison of pre- and post-treatment physical examinations, clinical laboratory tests, gastric antral biopsies and monitoring of adverse experiences. A statistically significant difference in gastric ulcer healing rate was seen at eight weeks among the treatment groups in the Intent-to-Treat Cohort: misoprostol 100 micrograms (62.0%), misoprostol 25 micrograms (50.0%), placebo (44.7%). The proportion of subjects healed in up to eight weeks of treatment was greatest in the misoprostol 100 micrograms group in all cohorts. Ulcer pain decreased in all treatment groups in successive weeks and there were no statistical differences among any of the three treatment groups. Diarrhea was the most frequently reported adverse experience: misoprostol 100 micrograms (9.8%), misoprostol 25 micrograms (7.7%), placebo (1.9%). The diarrhea was mild and self-limiting despite continued use of misoprostol. Overall evaluation of gastric antral biopsies showed no adverse changes in the morphology of the antral mucosa. We conclude that misoprostol 100 micrograms q.i.d. for up to eight weeks is safe and effective in the treatment of benign gastric ulcer.

Adult↗
PubMed1985

Inhibition of neurally mediated gastrin secretion by bombesin antiserum.

In vitro studies on the vascularly perfused rat stomach have shown that gastrin secretion is regulated by intramural cholinergic and noncholinergic neurons. We have postulated that bombesin (gastrin-releasing peptide), a known gastrin stimulant present in antral mucosal nerve fibers, is the most likely candidate for noncholinergic transmitter. Bombesin antiserum (final dilution, 1:150) but not control serum added to the vascular perfusate inhibited the gastrin response to 1,1-dimethyl-4-phenylpiperazinium by 59 +/- 17% (P less than 0.01) and to electrical field stimulation by 60 +/- 16% (P less than 0.01), and its effect was additive to that of 10(-7) M atropine (75-94%), thus accounting for the greater part of neurally induced gastrin secretion. The effects of atropine and bombesin antiserum on somatostatin secretion were consistent also with blockade of cholinergic and noncholinergic neurons, respectively. The results indicate that bombesin and acetylcholine are the main intramural neural regulators of gastrin and somatostatin secretion. Acetylcholine acts predominantly to decrease the paracrine secretion of somatostatin, thereby eliminating the continuous restraint of somatostatin on gastrin secretion and enabling bombesin to exert its potent stimulatory effect on gastrin secretion.

Acetylcholine↗
PubMed1984

Treatment of pyoderma gangrenosum with disodium cromoglycate.

The case of a 35-year-old black woman with a 10-year history of ulcerative colitis and a 3-year history of pyoderma gangrenosum is presented. The pyoderma gangrenosum was treated successfully with topical application of disodium cromoglycate.

Administration, Topical↗
PubMed1984

Effects of vasoactive intestinal peptide and secretin on gastrin and somatostatin secretion in the perfused rat stomach.

The presence of vasoactive intestinal peptide in intramural neurons of the stomach and in nerve fibers of antral and fundic mucosa raises the possibility that vasoactive intestinal peptide may participate in the regulation of gastrin secretion or somatostatin secretion, or both. This possibility was examined in the isolated vascularly perfused rat stomach by measuring the effects of vasoactive intestinal peptide and its homolog, secretin, alone or in combination with somatostatin antiserum on gastrin and somatostatin secretion. Both vasoactive intestinal peptide and secretin caused a sustained increase in somatostatin secretion in accordance with previous reports by others, but only secretin caused a sustained decrease in gastrin secretion; vasoactive intestinal peptide caused a transient increase in gastrin secretion followed by a return to control levels. Infusion of somatostatin antiserum in combination with vasoactive intestinal peptide caused a significant and sustained increase in gastrin secretion; however, the increase was not greater than that previously found with infusion of somatostatin antiserum alone. Infusion of somatostatin antiserum in combination with secretin caused a transient (2 min) increase in gastrin secretion followed by a sustained decrease in gastrin secretion equal to that caused by secretin alone. The results suggest that vasoactive intestinal peptide participates in the regulation of somatostatin but not of gastrin secretion. The results also suggest that basal secretion of somatostatin exerts an optimal inhibitory effect on gastrin secretion that is not exceeded by further increase in somatostatin secretion. At high concentrations, secretin has a direct inhibitory effect on gastrin secretion but this effect is not likely to be physiologically relevant.

Animals↗
PubMed1984

Stimulation of gastrin secretion in vitro by intraluminal chemicals: regulation by intramural cholinergic and noncholinergic neurons.

The regulation of gastrin and somatostatin secretion by intraluminal chemicals was examined in an isolated vascularly perfused rat stomach, a preparation that maintains the integrity of intramural neural pathways and the polarity of stimulation. Intraluminal perfusion with alkaline solutions (0.1 M NaHCO3) increased gastrin secretion, whereas perfusion with acid solutions (pH 3.5-3.0) inhibited gastrin secretion. Perfusion with 0.5% or 5% peptone solutions stimulated gastrin secretion and inhibited somatostatin secretion. Both these responses were abolished by addition of the axonal blocker, tetrodotoxin (10(-6) M), to the vascular perfusate, from which it was concluded that gastrin and somatostatin responses induced by peptone were mediated by intramural neurons. These neurons were both cholinergic and noncholinergic, because addition of an optimal dose of atropine (10(-7) M) to the vascular perfusate inhibited only partially the gastrin response and converted the somatostatin response from decrease below basal levels--a typical cholinergic effect--to significant increase above basal levels. As shown previously, atropine had an identical effect on gastrin and somatostatin responses to transmural electrical stimulation of the antral region. The results are in accord with a model for the regulation of gastrin secretion by intramural cholinergic and noncholinergic neurons. A direct effect of intraluminal chemicals on gastrin and somatostatin cells was not detected in this study, but is not precluded.

Animals↗
PubMed1982

Cholinergic and peptidergic receptors on isolated human antral smooth muscle cells.

Smooth muscle cells were isolated from segment so of human antrum obtained at operation. The presence, activity, and specificity of receptors to acetylcholine, the C-terminal octapeptide of cholecystokinin, methionine-enkephalin, and vasoactive intestinal peptide were examined. Muscarinic cholinergic receptors sensitive to low concentrations of atropine, cholecystokinin receptors sensitive to proglumide and dibutyryl cyclic guanosine monophosphate, enkephalin receptors sensitive to naloxone were demonstrated and found to mediate contraction. Vasoactive intestinal peptide receptors were demonstrated also and found to mediate relaxation. The stoichiometry and specificity of responses were closely similar to those previously found in isolated gastric smooth muscle cells of the guinea pig. The existence of high-affinity functional receptors on smooth muscle cells, together with the presence of the peptides in nerve terminals adjacent to these cells, makes it possible for these peptides to act as neurotransmitters.

Cholecystokinin↗
PubMed1981

Chlorpropamide-induced haemolytic anaemia.

A newly diagnosed diabetic patient, recently started on chlorpropamide, required emergency admission because of sudden onset of weakness and syncope. In vitro testing confirmed the diagnosis of chlorpropamide induced haemolysis, and withdrawal of the drug resulted in clinical recovery.

Anemia, Hemolytic↗
PubMed1981

Stimulation of gastrin and somatostatin secretion from the isolated rat stomach by bombesin.

The role of bombesin in the regulation of gastrin and somatostatin secretion was examined using an isolated vascularly perfused rat stomach preparation. Bombesin caused a biphasic, dose-dependent increase in gastrin and bombesin secretion. Neither somatostatin nor gastrin secretion was inhibited by atropine. The maximal gastrin response to bombesin (198 +/- 75% above basal levels) was less than one-half the maximal response to methacholine (462 +/- 94%). It was postulated that the concomitant release of somatostatin, in part from antral mucosa, attenuated the gastrin response to bombesin; the notion was tested with somatostatin antiserum. A 50- to 100-fold excess of sheep somatostatin antiserum augmented significantly the maximal gastrin response to bombesin by 966% in the initial peak period and by 532% in the plateau period; the response in the plateau period was not significantly different from the maximal response to methacholine. Methacholine stimulated the release of gastric bombesin also, but the exact cellular origin of the peptide could not be ascertained. On the basis of these results and of the topography of antral bombesin neurons and somatostatin D cells, a model for the neural (via bombesin) and paracrine (via somatostatin) control of gastrin secretion within the antrum is proposed.

Animals↗
PubMed1980

The value of endoscopy in the diagnosis of lymphoid nodular hyperplasia.

A 16-year-old boy was hospitalized because of abdominal pain, diarrhea, and weight loss. Serum immunoelectrophoresis showed an absence of IgA and diminished levels of IgM and IgG. Radiological examination of the upper gut was suggestive of lymphoid nodular hyperplasia, a diagnosis confirmed by endoscopy and intestinal biopsy. In addition, infestation with Giardia Lamblia was proven by duodenal aspirate at the time of endoscopy.

Adolescent↗
PubMed1980

Gastrin and somatostatin secretion by perfused rat stomach: functional linkage of antral peptides.

The isolated vascularly perfused rat stomach was used to study the polarity, kinetics, and stoichiometry of gastrin and somatostatin secretion and the interaction of the two antral peptides. The secretion of gastrin (79%) and somatostatin (95%) was predominantly in the circulation. Methacholine (5 x 10(-8) to 5 x 10(-4) M) produced a biphasic dose-dependent increase in gastrin secretion. The maximal gastrin response (434 +/- 89% above basal levels; P less than 0.001) was partially inhibited by 10(-8) M atropine and completely inhibited by 10(-7) M atropine. Methacholine produced a dose-dependent inhibition of somatostatin secretion; the inhibition was blocked by atropine. An inverse relationship between the secretion of gastrin and somatostatin was noted in the basal state and during infusion of methacholine or prostaglandin E2; the latter had effects on gastrin and somatostatin secretion opposite to those of methacholine. The data, together with data reported elsewhere that somatostatin antiserum stimulates gastrin secretion in the perfused stomach, are consistent with the hypothesis that gastric somatostatin secretion exerts a continuous restraint on basal gastrin secretion and that stimulation of gastrin secretion may be mediated in part by inhibition of somatostatin secretion.

Animals↗
PubMed1980

Neural release of vasoactive intestinal peptide from the gut.

The release of vasoactive intestinal peptide (VIP) from the canine gut and its possible neural origin were studied using two agents, oxytocin and neostigmine, known to increase peripheral levels of VIP. Oxytocin and neostigmine increased the portal concentrations of VIP by threefold and sevenfold, respectively. A considerable portal/femoral vein gradient ranging from twofold in the basal state to sevenfold during stimulation with neostigmine indicated that the gut was the main source of circulating VIP. The contribution of the brain was minor, and that of the uterus was undetectable. Release of VIP occurred from the entire gut: After enterectomy, the residual gut (stomach, pancreas, and proximal duodenum) released spontaneously a large amount of VIP which masked the effect of oxytocin. Tetrodotoxin and hexamethonium, but not atropine, inhibited oxytocin-stimulted release of VIP by 80% and 60% respectively. This prompted the conclusion that the release of VIP was predominantly neurally mediated and that the chain of transmission involved a preganglionic cholinergic pathway. Hexamethonium strongly inhibited neostigmine-stimulated release of VIP. Atropine was even more potent in that it abolished the effect of neostigmine. The effect of atropine was attributed to a blockade of ganglionic muscarinic receptors, which are preferentially activated by cholinesterase inhibitors like neostigmine. The results of this study and those derived from electrical stimulation of the vagus nerve are consistent with the hypothesis that circulating VIP is released from intrinsic neurons of the gut under preganglionic cholinergic control.

Animals↗
PubMed1979

Colonic involvement in salmonellosis.

Two cases of Salmonella colitis are described. Clinical and radiological differentiation from ulcerative colitis is difficult and necessitates repeated stool cultures. The management of Salmonella colitis is reviewed.

Adolescent↗