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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Disordered gastroduodenal motility may promote duodenal ulceration by allowing prolonged acid contact with the duodenal mucosa. Using a multilumen perfused catheter incorporating 3 pH microelectrodes, antral and duodenal pH and antropyloroduodenal pressure activity were recorded in 36 subjects (10 with healed duodenal ulceration, 11 with active duodenal ulceration, and 15 healthy volunteers) during fasting and after a radiolabeled solid test meal. Correct pH probe/catheter position was continuously verified by recording transmucosal potential difference across the pylorus. Patients with active and healed duodenal ulcer had similarly disordered gastroduodenal motility. The chief abnormalities consisted of an increase in postprandial duodenal retroperistalsis (healed duodenal ulceration, 12 +/- 1 events per hour; active duodenal ulceration, 12 +/- 1; control, 6 +/- 1; mean +/- SEM: healed and active duodenal ulceration vs. control, P = 0.004 and P = 0.03, respectively), a reduction in pressure waves sweeping aborally through the duodenum after the meal (healed duodenal ulceration, 22 +/- 4 events per hour; active duodenal ulceration, 23 +/- 3; control, 34 +/- 4: healed and active duodenal ulceration vs. control, P = 0.04 and P less than 0.05, respectively), and an increased incidence of atypical, complex forms of coordinated duodenal motor activity throughout the study (postprandial data; healed duodenal ulceration, 8 +/- 1 events per hour; active duodenal ulceration, 10 +/- 1; control, 4 +/- 1: healed and active duodenal ulceration vs. control, P = 0.02 and P less than 0.02, respectively). In addition, gastric emptying of the solid test meal was significantly delayed in healed, but not active, duodenal ulceration [half-emptying time, healed duodenal ulceration 185 minutes (117-235); active duodenal ulceration 102 minutes (80-200); control 107 minutes (78-130): healed duodenal ulceration vs. control, P less than 0.009]. Duodenal bulb pH was similar in controls and patients with active duodenal ulceration; however, bulb pH was less than 4 for a significantly greater period of time in healed duodenal ulceration compared with active ulcer patients, particularly after the meal. In conclusion, duodenal ulcer disease is associated with disturbed gastroduodenal motility, even when the ulcer is quiescent and when intraduodenal acidity is low. In healed duodenal ulceration, disturbed motility may promote ulcer relapse by impairing acid clearance from the bulb. However, in active ulceration other factors such as mucosal bicarbonate secretion may have a more influential role in determining intraduodenal pH.
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PMID:Disturbed gastroduodenal motility in patients with active and healed duodenal ulceration. 200 28

The objective of this study was to determine the in vitro corrosion products that resulted from crevice corrosion of low- and high-copper dental amalgams. Specimens were potentiostatically polarized in a chloride-containing electrolyte while set against a PTFE surface to form a crevice. After 16 h, corrosion products were examined by light microscopy, SEM, EDS, and XRD. Analysis showed the presence of three previously reported products [Sn4(OH)6Cl2, SnO, and Cu2O] and a new product, CuCl, which formed on high-copper, gamma 2-free amalgams. Thermodynamic considerations show that CuCl is stable for the reported in vivo potentials of amalgam restorations and the high acidity and high chloride ion concentration associated with crevice corrosion.
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PMID:Crevice corrosion products of dental amalgam. 206 90

The effects of two H2-receptor antagonists, famotidine and cimetidine, on the plasma levels of epidurally administered lignocaine were studied. Group A (n = 20) received famotidine 20 mg orally the night before surgery and 20 mg intramuscularly 60 minutes before induction of anaesthesia. Group B (n = 15) received cimetidine 200 mg orally the night before the surgery and 400 mg orally 60 minutes before the anaesthetic induction. Group C (n = 20) received neither famotidine nor cimetidine and served as controls. Twelve millilitres of 2.0% lignocaine with adrenaline 1:200,000 was injected into the epidural space in all patients, after the establishment of general anaesthesia with nitrous oxide, oxygen, and enflurane (0.3-0.5%). The patients who received cimetidine showed significantly higher plasma concentrations of lignocaine compared with either group A or group C at all investigation times (p less than 0.01). The mean peak plasma concentrations were 2.4 (SEM 0.1), 3.2 (SEM 0.2) and 2.3 (SEM 0.1) micrograms/ml in group A, B, and C, respectively. This study suggests that famotidine is preferable to cimetidine for control of gastric acidity before the use of lignocaine as the epidural anaesthetic.
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PMID:Effects of famotidine and cimetidine on plasma levels of epidurally administered lignocaine. 224 May 30

A new dental cement was developed by use of tetracalcium phosphate monoxide (Te-CP) and dicalcium phosphate dihydrate (DCPD). When an equimolar mixture of the two calcium phosphates was mixed with diluted phosphoric acid, it hardened into a phase of hydroxyapatite (HAp) resembling the main inorganic phase of hard tissues. The present study was undertaken to investigate physico-chemical properties of this newly developed apatite cement and to evaluate its potential as dental cement to clinical application. The setting time was reduced in the presence of synthetic HAp, indicating added HAp to be an accelerator in the setting reaction. The pH of paste rapidly increased to a neutral range from initial solution acidity of about 2.0 and the subsequent setting reaction proceeded in a neutral and weak alkaline pH range. The hardened solid 4 hours after saturation was identified as single phase of apatite by X-ray diffraction. The HAp crystallinity of the set cement varied with the crystallinity of HAp added as setting accelerator. The wet compressive strength of the cement stored for one day in synthetic saliva at 37 degrees C increased to 400 kg/cm2 as added HAp crystallinity decreased. Moreover no disintegration took place when the cement was stored at 37 degrees C in synthetic saliva, which was undersaturated with respect to DCPD but well supersaturated for HAp. In clinical application to animals, no significant cleavage was observed between the hard tissues and the cement by SEM even three months after the cement paste was filled in the tooth cavity of monkeys. In the specimen prepared one week after implantation in the medullary canal of rats, no inflammatory cell appeared. The specimen prepared one month after implantation showed that the set cement was tightly contacted with newly formed bone. These findings strongly suggest that the newly developed self-setting apatite cement is useful as a pulp capping agents, root canal fillings and bone substitute.
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PMID:[Studies on physico-chemical properties of self-setting apatite cement]. 256 62

Naturally occurring fogs are usually hypoosmolar with respect to body fluids and can be quite acidic. Because both hypoosmolarity and acidity can cause bronchoconstriction, we studied whether there was a positive interaction between these stimuli in 12 subjects with asthma. We administered the following aerosols: hypoosmolar saline (30 mOsm) at pH 5.5, 3 hypoosmolar acids (0.005 M H2SO4, 0.01 M HNO3 and a 1:1 mixture of 0.005 M H2SO4 and 0.01 M HNO3, all 30 mOsm) at pH 2, and isoosmolar 0.005 M H2SO4 (300 mOsm) at pH 2. Each aerosol was administered on a separate day and was inhaled through a mouthpiece during tidal breathing. Specific airway resistance (SRaw) was measured before and after the subjects inhaled aerosols delivered at as much as 5 doubling nebulizer outputs. For each aerosol challenge, an output-response curve was generated, and the nebulizer output required to increase SRaw by 100% above baseline (PO100) was calculated. Mean values of PO100 were significantly lower for each of the hypoosmolar acids than for hypoosmolar saline (1.65 + 0.43 g/min [mean + SEM] for saline compared with 0.95 + 0.11, 1.05 + 0.20, and 0.90 + 0.14 for H2SO4, HNO3, and a 1:1 mixture of the two; all p values less than 0.025). Mean values of PO100 did not differ among the 3 acids studied. For 7 of 12 subjects, all 3 acids caused a leftward shift in the output-response curve from the curve generated for hypoosmolar saline aerosol. Isoosmolar H2SO4 did not increase SRaw by 100% in any subjects, even at the maximal nebulizer output that delivered a concentration of H2SO4 in excess of 40 mg/m3.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Acidity potentiates bronchoconstriction induced by hypoosmolar aerosols. 284 38

Twenty-four hour intragastric acidity was studied in 27 healthy subjects (mean age = 29 yrs) by continuous recording in standardized conditions. Data obtained were expressed according to several analytical methods as used extensively elsewhere. In our study, there was a wide discrepancy in results from one subject to another. The use of median values of pH was more appropriate than mean values to express half-hour acidity levels for 24 hours. The median value of H+ concentration is recommended as well. The median value of pH varied from 1 to 4.8 with a slight rise during the second half of the night. During the postprandial period, increase of pH values was prolonged over 2 h 30 in 50 p. 100 of subjects. Profile of pH allowed to demonstrate the distribution of pH value without excluding the extreme values. Both periodicity of pH measurement (30 or 60 min) and parameters used to quantify acidity (percentage of time or pH value at or below threshold values) did not modify results. As measured over a 24 hours period, the percentage of time (mean +/- SEM) at or below pH 1.5 and 3.5 was 54 +/- 3 p. 100 and 85 +/- 2 p. 100, respectively. Daytime and night-time profiles were similar. Mean 24 h H+ concentration (mean +/- SEM) was 47 +/- 35 mmol/l, with, once again, similarity between day and night-time values. The mean 24 h pH values underestimated true acidity with respect to median values.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[How to express results of 24-hour gastric pH measurement? Choice of a mode of expression in 27 healthy subjects]. 280 8

The effect of pirenzepine on 24 hour intragastric acidity was studied in 10 healthy volunteers using ambulatory 24 hour intragastric pH-monitoring in a double blind crossover study. Tests were performed on the seventh day of ingestion of either placebo, 75 mg pirenzepine or 150 mg pirenzepine per day. The drugs were given at two doses at 8.30 am and 8.30 pm. Mean nocturnal hydrogen ion activity during placebo treatment was 68 mmol/l +/- 9 SEM and was reduced by 75 mg (26%, p less than 0.01) and 150 mg of pirenzepine (36%, p less than 0.01), respectively. Mean diurnal hydrogen ion activity was 32 mmol/l +/- 6 SEM and was not significantly reduced (p greater than 0.1) by either dose of pirenzepine (4% and 12% respectively). Thus, the effect of pirenzepine on intragastric acidity is small, even with high doses of the drug, and becomes apparent only during the night.
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PMID:Evaluation of pirenzepine on gastric acidity in healthy volunteers using ambulatory 24 hour intragastric pH-monitoring. 388 25

Fasting serum gastrin has been measured by radioimmunoassay in 72 patients with duodenal ulcer and compared with that in normals, patients with gastric ulcer, and with the Zollinger-Ellison syndrome. The mean (+/- SEM) gastrin levels were 15.7 +/- 1.5 pg/ml in the duodenal ulcer group, 32.1 +/- 4.3 pg/ml in normals, 118 +/- 18.1 pg/ml in gastric ulcer, and between 450 and 2,000 pg/ml in the Zollinger-Ellison syndrome. There were no difficulties in distinguishing simple ulcer from the Zollinger-Ellison syndrome as the presence of hyperchlorhydria in combination with hypergastrinaemia led to a confident diagnosis of the latter disease.The effect of protein, glucose, and cream feeding with and without atropine was also assessed in a group of these patients with duodenal ulcer. As in normals, there was no stimulation of gastrin release by either atropine alone, distilled water, glucose, or cream. However, protein alone produced a greater rise in serum gastrin levels compared with that in normals and prior atropinization augmented this response greatly in duodenal ulcer. This indicates an increased amount of releasable gastrin in the latter disease, the release of which, under basal conditions, is suppressed by the high acidity in the antrum.
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PMID:Serum gastrin in duodenal ulcer. I. Basal levels and effect of food and atropine. 513 20

Ranitidine 150 mg was given to 126 patients requiring elective Caesarean section under general anaesthesia: 43 women had ranitidine alone, 43 had this supplemented by a pre-induction dose of sodium citrate and 40 patients had ranitidine plus sodium bicarbonate. All three sub-groups provided satisfactory gastric pH and volume. Ranitidine 150 mg was given orally every 6 hours to women in labour. Of 221 patients requiring general anaesthesia during labour, 103 women received 30 ml 0.3 M sodium citrate and 118 women, 20 ml of 8.4% sodium bicarbonate 10 minutes before induction of anaesthesia. In the citrate sub-group there was one patient with a gastric pH less than 2.5 (mean pH 6.2, SEM 0.13 range 2.1-8.4). In the bicarbonate sub-group the lowest gastric acidity was 3.8 (mean pH 8.3, SEM 0.11 range 3.8-9.83).
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PMID:Combined treatment with ranitidine and saline antacids prior to obstetric anaesthesia. 609 96

The influence of oral carbenoxolone sodium (50 mg X 3 daily) on prostaglandin E2 release into gastric juice has been examined in nine peptic ulcer patients (duodenal ulcer, n = 6; prepyloric ulcer, n = 1; gastric ulcer, n = 2) during modified sham feeding and following bolus stimulation of acid secretion by pentagastrin (6 micrograms/kg). Carbenoxolone increased the overall mean of prostaglandin E2 concentrations in gastric juice following modified sham feeding by 32 +/- 9% (mean +/- SEM; P less than 0.02) and decreased the acidity slightly but significantly (P less than 0.05). A marked rise in prostaglandin E2 levels (46 +/- 11%; n = 5; P less than 0.02) was observed in for duodenal ulcer patients and the patient with a prepyloric ulcer responding to therapy (i.e., pain relief and ulcer healing within 4 weeks of treatment). A significant peak (P less than 0.05) related to modified sham feeding was observed only during medication, while a late gradual increase in prostaglandin E2 levels--not associated with vagal stimulation--occurred both in control and carbenoxolone experiments. No significant differences were observed following pentagastrin stimulation. The initial peak in prostaglandin E2 levels observed during medication favours the notion that the mechanism of drug action relies on inhibition of enzymatic degradation while the late increase in prostaglandin E2 levels may be explained by artificial prostaglandin formation during the aspiration procedure.
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PMID:Effect of carbenoxolone on gastric prostaglandin E2 levels in patients with peptic ulcer disease following vagal and pentagastrin stimulation. 641 22


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