Helion-neon and infra-red laser do not modify the U.V.A. and U.V.B. minimal erythema dose.
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Adolescent↗
Biomedical subjects
E Molina
Publications and source records attributed to E Molina.
Glucose tolerance in chronic alcoholics after alcohol withdrawal: effect of accompanying diet.
The effect of alcoholism or acute alcohol ingestion on carbohydrate metabolism is not clear. The metabolic features of alcoholics cannot be easily achieved in normal men submitted to investigations concerning the effects of alcohol on glucose tolerance. Undernutrition and/or malnutrition characterize the eating behavior of alcoholics. It is also well-known that diet is an important determinant of carbohydrate tolerance. Thus, we studied the effects of a controlled diet on glucose tolerance and insulin release in a group of chronic alcoholics, with or without withdrawal from alcohol. Twenty-two subjects took part in the study; their mean caloric intake was 2,805 +/- 91 kcal/d, 58% of which was due to alcohol. In all subjects five days after an isocaloric diet and no alcohol, we performed an oral glucose tolerance test (OGTT). After that, the subjects were divided into three subgroups: group A, eight subjects with alcohol withdrawal and an 17.5 kcal/kg/d diet; group B, eight subjects with alcohol withdrawal and a 35 kcal/kg/d diet, and group C, six subjects with a 35 kcal/kg/d diet plus ethanol 200 g/d. After 3 weeks a second OGTT was performed. We found a significant improvement of the glucose tolerance and of the release of insulin in group B as well as group C; the alcohol withdrawal per se was irrelevant to the observed modifications of the glucose tolerance. Our data suggest that a poor diet would be a major cause of carbohydrate intolerance in alcoholics.
Adult↗
Mediastinitis after whiplash injury.
The authors describe a rare complication of whiplash injury. Diffuse mediastinitis resulted from extension of a whiplash-induced retropharyngeal abscess into the thorax. Early diagnosis of the cervical infection was masked by the simultaneous presence of infectious mononucleosis. Aggressive surgical management including bilateral thoracotomy was required to resolve the septic course. A review of the literature discusses the pathogenesis of this complication including the route of extension into the mediastinum and supports the use of aggressive surgical therapy to reduce the associated mortality.
Adult↗
Bombesin and G-17 dose responses in duodenal ulcer and controls.
Gastric acid and pepsin secretion and serum gastrin concentrations were measured in nine patients with uncomplicated duodenal ulcer (DU) and 10 normal controls in the fasting state and in response to graded doses of bombesin, a tetradecapeptide gastrin releaser, and, for reference, synthetic gastrin G-17. Serum gastrin with bombesin stimulation was significantly greater in duodenal ulcer (maximum 467 pg/ml) than in controls (153 pg/ml), while in seven of the DU group tested gastrin levels after a meal were not different from that seen in five of the normal controls. Gastric acid concentrations and outputs were greater in duodenal ulcer with both stimuli. Secretory responses were then related to serum gastrin levels; despite increasing gastrin levels with bombesin stimulation, peak outputs achieved with bombesin were only 50% of G-17 maximum in normals and up to 90% of maximum in duodenal ulcer. Up to the point of peak response to bombesin, acid and pepsin outputs were the same with exogenous and endogenous gastrin, ie, bombesin acted only via G-17. Furthermore, in direct comparison of duodenal ulcer and normals with G-17 infusion, acid and pepsin outputs related to serum gastrin were congruent up to 75% of duodenal ulcer maximum, at which point normals reached their maximum level. These data have shown that duodenal ulcer patients are not more sensitive to either exogenous or endogenous gastrin; we have also shown regulatory defects in duodenal ulcer patients not previously described: an exaggerated release of gastrin with bombesin stimulation, and a defective inhibition of acid and pepsin secretion with higher doses of bombesin.
Adult↗
Comparison of the effects of structurally different H2-antagonists on acid and pepsin activity stimulated by dimaprit in conscious cats.
In the present study the effects of three structurally different H2-receptor antagonists (cimetidine, ranitidine and oxmetidine) have been investigated on gastric acid and pepsin secretion of eight cats provided with cannulated gastric fistulas. The maximum pepsin output obtained from a set of complete dose-response curves of dimaprit was not statistically different from basal values. In the presence of the H2-antagonists, while the gastric acid secretion induced by dimaprit was competitively antagonized, the pepsin secretion was differently affected. The data obtained on pepsin activity with cimetidine and ranitidine were quite similar to the control values. By contrast, oxmetidine induced a significant increase. The results suggest a very weak involvement of the H2-receptors in pepsin activity and that oxmetidine performance could not be attributable to an H2-receptor block.
Animals↗
Effects of very low doses of atropine on basal acid and pepsin secretion, gastrin, and heart rate in normals and DU.
Muscarinic mechanisms in basal acid and pepsin secretion in man were quantitated by graded intravenous doses of atropine (1-16 micrograms/kg). Secretion was dose-responsively inhibited in six healthy controls. For the mean dose response, maximum inhibition (Imax) was 100%, and D50 (dose inhibiting 50%) was 0.31 +/- 0.06 and 0.93 +/- 0.13 micrograms/kg, respectively, for acid and pepsin. In 24 patients with duodenal ulcer (DU), calculated Imax was also 100%, and D50S were 1.2 +/- 0.27 and 1.7 +/- 0.3 micrograms/kg, respectively. The low D50 values and the 100% calculated maximum inhibition indicated that in both groups basal secretion was largely or completely cholinergic dependent. We also found that atropine raised heart rate in controls by 44 +/- 1 beats per min (bpm) (D50 = 6 +/- 1.1 micrograms/kg), while the mean maximum increase in DU was only 23 +/- 2 bpm (P less than 0.01) with (D50 = 5.3 +/- 1.0 micrograms/kg (NS)). In DU atropine increased fasting serum gastrin from 62 to 82 pg/ml (P less than 0.05); the increase in normals from 32 to 38 pg/ml was not significant. Thus, while both normals and DU exhibited the same qualitative responses to muscarinic receptor antagonism by atropine with respect to gastric secretion, gastrin levels, and heart rate, there were quantitative differences in all three parameters.
Acetylcholine↗
[4-[Benzyl-(2-dimethylaminoethyl)amino]pyrimidine compounds with selective antagonistic activity against H1-histamine receptors].
This paper describes the synthesis of 2- and 4-[benzyl-(2-dimethylaminoethyl)amino]pyrimidine compounds and their antihistaminic properties studied on isolated guinea-pig ileum. Calculated pA2 values show that the antihistaminic activity of 4-[p.methoxybenzyl-(2-dimethylaminoethyl)amino]pyrimidine is specific and potent (8-10 times higher than that of thonzylamine).
Acetylcholine↗
[Segmental dilatation of the ileum].
Three cases of segmental dilatation of ileum surgically are presented. Authors have reviewed medical literature since the first case reported in 1959, and have been able to collect 33 cases. Although it is considered an identical entity involving either colon or small bowel, clinical picture and age of presentation are different. Cases involving the colon have a clinical picture very similar to that of Hirschsprung's disease, usually appearing in the lactancy or later on. Cases involving ileum or jejunum usually are manifested as a neonatal bowel obstruction. Pathological examination shows a bowel wall with all his layers as well as a normal ganglion cells. Surgical resection of dilated intestinal segment is curative.
Dilatation, Pathologic↗
Effect of cimetidine on histamine-stimulated gastric acid and electrolytes in dogs.
Intravenous administration of cimetidine (0.25-2.0 mg X kg-1 X h-1) inhibited histamine-stimulated gastric acid secretion in both intact (Ki = 1.0 mg X kg-1 X h-1) and vagotomized (Ki = 1.75 mg X kg-1 X h-1) dogs. During histamine infusion, all doses of cimetidine reduced gastric volume output; high doses increased gastric juice pepsin and [Na+] and reduced [H+] and [Cl-]. Gastric juice [K+] was not affected during cimetidine infusion. The cimetidine-induced changes in electrolyte concentrations were qualitatively comparable with those observed on withdrawal of histamine stimulation. On termination of cimetidine infusion with continued histamine administration, gastric [K+] and volume output increased immediately, followed 30 min later by an increase in [H+] and a reciprocal decrease in [Na+]; [Cl-] did not recover. The changes in gastric juice electrolytes after termination of cimetidine, with the exception of [Cl-], mimicked the changes observed on initiation of histamine stimulation. These data indicate that the effects of cimetidine may be totally explained by its antagonism of histamine binding to the parietal cell H2-receptor, that vagotomy reduces cimetidine binding to the H2-receptor, and that cimetidine antagonism of histamine is rapidly reversed on removal of the antagonist.
Animals↗
Relation of gastric acid and pepsin secretion to serum gastrin levels in dogs given bombesin and gastrin-17.
To quantitate bombesin stimulation of gastric acid and pepsin via release of gastrin, five gastric fistula dogs were given graded doses (60-1,250 pmol X kg-1 X h-1) of bombesin tetradecapeptide and 40-2,000 pmol X kg-1 X h-1 of synthetic gastrin-17 (G-17). Acid and pepsin output and serum gastrin were proportional to the dose of stimulant. The half-maximal dose of bombesin for gastrin release was 200 pmol X kg-1 X h-1. Bombesin-stimulated acid secretion related to serum gastrin concentrations was congruent with the G-17 curve, but with a maximum of only 62% of the G-17 maximum before declining by 27% despite higher serum gastrin levels. This suggested that bombesin stimulates acid secretion only via gastrin release and inhibits at higher doses by releasing another inhibitory peptide, most likely somatostatin, which is also released by bombesin. The same mechanism could apply to supramaximal inhibition of acid and pepsin seen with high doses of G-17. Because the pepsin curve related to serum gastrin was to the left of the G-17 curve, we concluded that another secretagogue released by bombesin acts synergistically with gastrin on pepsin secretion. Therefore, bombesin stimulates gastric secretion through gastrin release, but its effects are modified by peptides coreleased to a) increase pepsin output at low doses and b) limit the output of acid and pepsin to 50-60% of the G-17 maximum.
Animals↗
Effects of four H2 histamine antagonists on bethanechol-stimulated acid and pepsin secretion in the dog.
In five gastric fistula dogs, each of four H2-receptor antagonists was given (at doses roughly equal to the dose inhibiting histamine stimulation at 50%) as background infusion to graded doses of i.v. bethanechol. We measured acid and pepsin secretion and gastrin release. All four compounds noncompetitively inhibited acid secretion, reducing maximum acid outputs by 50 to 70%. Two compounds, tiotidine and cimetidine, shifted the bethanechol dose-response for pepsin secretion about 30% to the right at midpoint without reducing maximum output significantly, whereas the other two, ranitidine and metiamide, did not alter the dose-response. Dose-dependent gastrin release was unaffected by cimetidine, an imidazole compound, and augmented by tiotidine and ranitidine, the two nonimidazole compounds. Actions on pepsin and gastrin are thus not related to H2-receptor effects. The uniform effect of the four antagonists on acid secretion indicates an essential interaction between cholinergic and histamine effects on the parietal cell, although we could not distinguish between prereceptor, receptor and postreceptor sites for such interaction.
Animals↗
Effects of pirenzepine and atropine on vagal and cholinergic gastric secretion and gastrin release and on heart rate in the dog.
To characterize and quantitate pathways of stimulation of gastric secretion via vagal excitation induced by 2-deoxy-D-glucose, we used graded doses of the two muscarinic antagonists, atropine and pirenzepine. Studies were performed in four conscious gastric fistula dogs with antral vagotomy to eliminate the gastrin release component of the vagal response. To further localize the site of action of the antagonists, both were tested against bethanechol, which stimulates secretion at postganglionic sites. Acid and pepsin secretion stimulated by either bethanechol or the vagus were inhibited in a dose-responsive manner by both atropine and pirenzepine, which displayed similar potencies. These data indicate that: 1) the vagus acts on the gastric fundus solely via muscarinic receptors; 2) the muscarinic receptors controlling gastric secretion are of the high-affinity (M-1) subtype; and 3) the vagus is very sensitive to atropine with D50 less than 1.4 nmol/kg. Heart rate was increased up to 120 beats/min above the resting rate by atropine; half-maximal increase was calculated to occur at 10 nmol/kg (ED50). Pirenzepine had a much less potent effect on the heart; the ED50 was 200 to 300 times greater than that for atropine. These data indicate that heart rate is affected by a mechanism acting via a muscarinic receptor pathway that has a low affinity for pirenzepine (M-2 receptor subtype).
Animals↗
Anticholinergic potency of diphenhydramine (Benadryl) measured against bethanechol in the gastric fistula dog.
We quantitated the gastric secretory anticholinergic effect of diphenhydramine (Benadryl) against graded doses of bethanechol, a cholinergic agonist, which was used to stimulate acid and pepsin secretion. Anticholinergic potency of diphenyhydramine was 10,000 times less than that reported for atropine and was 1,000 times less than the reported potency of diphenhydramine antagonism of histamine H-1 effects.
Animals↗
[Gastric acidity and serum levels of pepsinogen I and gastrin in children with primary duodenal ulcer].
A population of 8 children aged 7 to 13 and radiologically and/or endoscopically diagnosed of duodenal ulcer is compared with another made up of 12 normal children of similar ages and weights. In both groups gastric secretion, basal and after pentagastrin stimulation, and serum levels of gastrin and pepsinogen I, basal and after pentagastrin stimulation, and serum levels of gastrin and pepsinogen pepsinogen basal and after pentagastrin stimulation, and serum levels of gastrin and pepsinogen I, basal and after proteic meal, were studied. BAO, MAO and PAO were significantly higher in ulcer patients. Gastrinemia, both basal and stimulated, were rather similar in both groups. Serum pepsinogen I was always higher in ulcer patients in the basal state than in their healthy counterparts (greater than ng/ml vs. 30-50 ng/ml), but was not modified by proteic meal in either group. The fact that all ulcer children had a familial history and a basal pepsinogen I elevated, aside with the secretory response to stimulation, suggests that ulcer can be result either of an increased mass or of a higher sensitivity of gastric parietal cells that could be related to genetic factors.
Adolescent↗
Food and pentagastrin stimulation of gastrin, pepsinogen I and acid in children with primary duodenal ulcer.
Six cases of duodenal ulcer were studied in male children (mean age 8.8 yrs., range 6-12 yrs., mean weight 29.8 kg). All were submitted to X-ray examination and/or digestive endoscopy. Ten healthy children, matched by weight, age and sex were chosen as controls. All children underwent a standardized protein meal to evaluate serum gastrin and pepsinogen I response and the pentagastrin test for acid secretion. The serum gastrin level was found to be similar in the two groups (normal children and duodenal ulcer) both in the fasting state and after food stimulation, whereas the basal and after-meal serum pepsinogen I values were statistically higher in the duodenal ulcer group (p less than 0.01). The pentagastrin test showed a basal, maximal and peak acid output significantly lower in controls than in the subjects with primary duodenal ulcer. The results confirm that elevated gastric acid response is already present in duodenal ulcer of childhood and seems to be its cause rather than its consequence. Our finding of an already elevated pepsinogen I level, coupled with the already reported family histories of the disease, further support an inherited basis for duodenal ulcer in childhood.
Child↗
Inhibition of basal acid, chloride, and pepsin secretion in duodenal ulcer by graded doses of ranitidine and atropine with studies of pharmacokinetics of ranitidine.
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Adult↗
Analysis of the 2-deoxy-D-glucose-induced vagal stimulation of gastric secretion and gastrin release in dogs using methionine-enkephalin, morphine and naloxone.
Gastric acid and pepsin secreted in 3 hr and antral gastrin released in response to vagal excitation induced by 2-deoxy-D-glucose (2DG), 625 mumol/kg i.v., were studied in six conscious trained gastric fistula dogs. During a 2-hr infusion, Met-enkephalin (96 nmol/kg/hr; delta receptor) reduced the 2DG response by 50%; when the enkephalin was stopped there was a rapid rebound to peak values. Met-enkephalin also blocked the release of gastrin in the first 15 min. By itself, Met-enkephalin did not stimulate secretion and slightly depressed gastrin. By contrast, morphine (96 nmol/kg/hr; mu receptor) augmented and sustained the 2DG gastric acid secretory response. This effect was blocked by naloxone. Morphine alone caused a small rise in serum gastrin after 90 min, followed by a delayed gastric acid secretion of about 30% of the peak 2DG response. Naloxone, a mu opiate antagonist (mu/delta, 27:1), also inhibited the 2DG gastric secretory response by about 50% and augmented the Met-enkephalin inhibition of secretion without blocking either the secretory rebound or the effect on gastrin release. None of the three opiates changed the direct cholinergic gastric secretory or gastrin-releasing effects of bethanechol. Thus, vagal stimulation of the stomach involves pathways which can be influenced by both mu and delta opiates, with apparently opposite effects, proximal to the level of acetylcholine action on the gastric mucosa. The central and peripheral control points in the activation of the stomach via the vagus which are sensitive to opiates have yet to be located and explained.
Animals↗
Identification of a particular B cell alloantigen associated with susceptibility to lepromatous leprosy.
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Adolescent↗