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Effect of acid perfusion of the terminal ileum on plasma immunoreactive secretin and pancreatic secretion in the rat.

The distribution of immunoreactive secretin in acid extracts of the alimentary tract of the rat was determined. It was found to be contained in higher concentrations in the duodenum and in the terminal ileum than in other parts of the intestine. To elucidate the possible role of secretin contained in the terminal ileum, this part of the intestine was perfused with hydrochloric acid, a potent secretin secretagogue, and changes in plasma immunoreactive secretin levels and in pancreatic secretion were investigated in anaesthetized rats. Plasma immunoreactive secretin was increased from 65 +/- 5 pg/ml to 108 +/- 13 pg/ml during a 10 minutes perfusion with hydrochloric acid. This was significantly higher than that of saline perfusion but significantly lower than that of duodenal perfusion with hydrochloric acid. Acid perfusion of the terminal ileum also caused a three-fold increase in pancreatic flow rate and a twofold increase in bicarbonate concentration. These results suggest that the terminal ileum, through release of secretin, might play a role in regulating the pancreatic secretion of water and bicarbonate in response to changes in intraluminal fluids in the distal intestine in the rat.

Animals↗

[Influence of an acute hypercalcemia on the gastric secretion in duodenal ulcer, peptic ulcer of the jejunum and Zollinger-Ellison syndrome].

In 36 patients with ulcer without Zollinger-Ellison-syndrome (25 patients with recurrent duodenal ulcer, 11 with an ulcus pepticum jejuni after B II-resection of the stomach) and 2 patients suffering from ulcus pepticum jejuni with an ascertained gastrinoma the secretion of acid was compared after stimulation of pentagstrin (6 mug/kg) and calcium (4 mg Ca++/kg/h). The secretion of hydrochloric acid was statistically significantly stimulated in all patients suffering from ulcer by the hypercalcaemia (increase of the serum calcium concentration from 5.0 +/- 0.3 mval/1 to 6.2 +/- 0.8 mval/1). But in patients suffering from ulcer with gastrinoma the stimulatory effect was larger than in such patients without autonomous source of gastrin: the calcium-stimulated secretion of hydrochloric acid was on the average in cases of duodenal ulcer 40% (2 to 68%), in the ulcera peptica jejuni 47% (17 to 75%), in the 4 comparative examinations of the two patients with Zollinger-Ellison-syndrome, however, always more than 100% (106 to 177%) of the pentagastrin-stimulated peak secretion. The comparative test of the pentagastrin and calcium-stimulated secretion of hydrochloric acid could be a help for the proof of autonomous places of the formation of gastrin.

Acute Disease↗

Effect of roxatidine acetate on daytime and night-time peptone-stimulated gastric acid secretion.

A double-blind, randomised, crossover study in 12 healthy volunteers was performed to assess the effects of roxatidine acetate 75 mg or placebo administered at 8 am and 9 pm on peptone-stimulated hydrochloric acid secretion. In comparison to placebo, roxatidine acetate produced an average reduction of daytime hydrochloric acid output of 86% and 32%, respectively, for the 4- to 6-hour and 10- to 12-hour post-drug administration phases. In addition, roxatidine acetate produced reductions in nocturnal hydrochloric acid output of 75 to 92% with an associated rise in intragastric pH of around 2 units compared to placebo. No side effects or clinically significant alterations in haematological or biochemical values were reported following roxatidine acetate administration. These results suggest that roxatidine acetate is a potent and effective inhibitor of day and night-time intragastric acid secretion.

Adult↗

Regionally perfused fatty acids augment acid-induced canine pancreatic secretion.

To study interactions between hydrochloric acid and fatty acids on pancreatic secretion, six dogs with chronic gastric, pancreatic, and small intestinal cannulas received various combinations of the following intestinal perfusates: 20, 40, and 80 mM hydrochloric acid, oleate, dodecanoate, or 0.15 M saline. Regional intestinal perfusion (a proximal segment measuring 45 cm from the pancreatic duct versus the remaining small bowel) was utilized to separate the aqueous acid and lipid solutions. Both oleate and dodecanoate augmented the bicarbonate output induced by intraluminal acidification. In other experiments, intraluminal oleate, when combined with exogeneous intravenous secretin (12.5-900 ng . kg-1 . h-1), potentiated the secretin-induced bicarbonate output at low secretin doses. Dodecanoate also increased secretin-induced bicarbonate output. In all of these studies, protein outputs were increased by intestinal fatty acids. It is concluded that intestinal fatty acids can enhanced acid-induced canine pancreatic secretion.

Animals↗

Reversed-phase high-performance liquid chromatographic determination of tetracyclines in urine and plasma.

The high-performance liquid chromatographic separation and quantitative analysis of oxytetracycline, tetracycline, and chlortetracycline from urine and plasma were effected on an octadecylsilane reversed-phase packing. The calcium complexes of the tetracyclines were extracted from urine and plasma with ethylacetate and then reextracted into hydrochloric acid. Following the injection of the hydrochloric acid extracts onto the column, the individual tetracyclines were eluted isocratically and quantitated spectrophotometrically. Concentrations of less than 1 microng/ml in urine and 1.5 microng/ml in plasms were quantitatively determined with a relative standard deviation of less than 5%.

Animals↗

Bile salt-induced injury of rabbit oesophageal mucosa measured by hydrogen ion disappearance.

Oesophageal injury secondary to gastro-oesophageal reflux is unlikely to be due to the effects of hydrochloric acid alone. The present authors have investigated the development of acid and bile salt-induced oesophageal mucosal injury in a rabbit model. Solutions of hydrochloric acid and sodium taurocholate (ST) were perfused through an isolated oesophageal preparation and mucosal injury was determined by measuring the rate of H+ disappearance. Perfusion with acid alone in concentrations up to 10 mmol/l did not affect the H+ disappearance rate. Addition of 1 mmol/l ST to an acid perfusate resulted in loss of H+ from the system. The increase in H+ disappearance rate was associated with loss of ST from the perfusate. Sodium taurocholate was only lost from the system when in an acid medium. Increased rate of H+ disappearance occurred even after the bile salt had been washed out of the perfused oesophagus. The mechanism of bile salt-induced mucosal injury was unlikely to be due to mucosal disruption secondary to micelle formation since the critical micellar concentration of taurocholate was found to be greater than that used in the perfusate. These findings indicate that bile salts may be an important factor in hydrochloric acid-related damage to oesophageal mucosa, by acting through mechanisms unrelated to micelle formation.

Animals↗

Hypersensitivity to acid in ulcer-like functional dyspepsia.

OBJECTIVES: The mechanism of pain sensation in patients with ulcer-like functional dyspepsia is unclear and there are no guidelines for its treatment. Whilst much research and many pharmacological treatments have provided symptomatic relief of ulcer-like functional dyspepsia through control of acid secretion, the role of acid in ulcer-like functional dyspepsia is unknown. We carried out this study to investigate the role of hypersensitivity to acid in the sensation of pain in ulcer-like functional dyspepsia by direct administration of acid into stomach. METHODS: Twelve patients with ulcer-like functional dyspepsia (5 male, 7 female, mean age 41.0 years old, 7 with mild chronic superficial gastritis, 2 with metaplastic gastritis and 3 with normal endoscopic findings) and seven healthy control subjects (3 male, 4 female, mean age 36.0 years old, 7 with normal endoscopic findings) participated in the study. After overnight fasting, a nasogastric sump tube was inserted and its tip was positioned in the antrum under fluoroscopic guidance. Normal saline or 0.1N hydrochloric acid was administered in random and single blind cross over fashion. The test was considered positive only if similar pain developed-similar to that experienced by the patient under nonstudy condition- during the administration. RESULTS: Five patients (41.7%) developed pain with 0.1N hydrochloric acid administration, but none with normal saline (p < 0.05). None of the healthy controls developed pain upon administration of 0.1N hydrochloric acid or normal saline. CONCLUSION: We suggest that acid hypersensitivity plays a role in the sensation of pain in ulcer-like functional dyspepsia.

Adult↗

Determination of superabsorbent polyacrylate dust in workplace atmospheres after derivatization with ethanol and using HPLC with pulsed electrochemical detection.

Superabsorbent polyacrylates (SAPs) have been used in the hygiene industry for many years. A derivatization and analytical method was developed for routine analysis of trace levels of SAP dust in workplace atmospheres. In comparison with existing methods, which are based on the sodium content or the ion exchange properties of the polymer, this method is more specific. It has the advantage of not being influenced by any sodium containing contaminants. Air samples are collected on Teflon filters using air monitoring sampling cassettes. The filters are subsequently placed in quartz vials and a reaction mixture containing hydrochloric acid in ethanol is added. The hydrochloric acid-ethanol solution, when heated, converts the carboxylic acid groups on the backbone of the insoluble polyacrylate into ethyl esters. After reaction, the excess of ethanol and hydrochloric acid is completely removed under vacuum. The sample is then treated with aqueous sodium hydroxide at 80 degrees C to release the bound ethanol. The solution is analyzed by HPLC on an anion exclusion stationary phase using dilute perchloric acid as mobile phase. Ethanol is identified and quantified with a pulsed electrochemical detector. Several environmental samples in addition to laboratory spiked samples were successfully analyzed with this technique. Recoveries averaged > 85% for spiked blank filters at levels from 5 to 50 micrograms per filter with relative standard deviations up to 7%. The instrument's limit of detection (LOD) for ethanol was 0.1 mg l-1. The LOD for derivatization and analysis corresponds to 3 micrograms of SAP per filter (assuming an esterification factor of 0.30 microgram of ethanol per microgram of SAP).

Acrylates↗

Motilin secretion and the migrating myoelectric complex in the pig.

The concentration of motilin in plasma from the abdominal aorta and the hepatic portal vein and the net portal motilin output varied with the phase of the migrating myoelectric complex (m.m.c.) in five of six pigs fasted for 17 h. Maximum concentrations and output occurred 9-12 min before phase III in the duodenum or upper jejunum. In fed pigs m.m.c.s occurred and the first phase III in the duodenum occurred within 90 min of feeding. Both portal and arterial motilin concentrations were reduced after feeding and no longer varied with the phase of the m.m.c. Altered secretion of motilin after feeding did not appear to be associated with absorption of glucose as infusion of glucose (50 g/l, 10 ml/min) into the duodenum raised arterial and portal plasma glucose concentrations to post-prandial levels yet motilin concentrations and output rates still varied with the phase of the m.m.c. Infusions of motilin (1 or 10 ng/kg X min) into the portal vein of 17 h fasted pigs did not induce an extra phase III or alter the duration of the m.m.c. Hydrochloric acid (100 mmol/l) infused into the duodenum of fasted pigs at 10-21 ml/min increased the concentration of motilin in the portal blood but was without effect at 5 ml/min. Rapid injections of 50 ml hydrochloric acid into the duodenum also increased the portal motilin concentration. Hydrochloric acid infusion or injection did not alter the interval between phase IIIs. It is concluded that motilin secretion is a consequence of the m.m.c. or shows the same periodicity as the m.m.c. but that motilin is not an important factor in the initiation and control of the m.m.c. in the pig.

Animals↗

Decomposition rate of hydrogen peroxide bleaching agents under various chemical and physical conditions.

The decomposition rate of 30% hydrogen peroxide was measured when hydrogen peroxide was mixed with 36% hydrochloric acid and anaesthesia either in 5:5:1 solution and in a solution of 20% sodium hydroxide at temperatures of 16 degrees to 20 degrees C and at 45 degrees C, respectively. The effect of ferris chloride on the decomposition of hydrogen peroxide was also observed. The decomposition of 30% hydrogen peroxide in sodium hydroxide solution was faster than that in the mixture of hydrochloric acid and ether at low temperature (16 degrees to 20 degrees C). The decomposition of hydrogen peroxide was accelerated by heat. The experiment implies that the bleaching effect of hydrogen peroxide can be achieved without heat by use of a sodium hydroxide solution. Further study on the rationale of the compound of the McInnes solution (hydrogen peroxide, hydrochloric acid, and anaesthesia ether mixed at a ratio of 5:5:1) is needed.

Chemical Phenomena↗

Increased pulmonary vascular permeability following acid aspiration.

The effect of hydrochloric acid aspiration on transvascular fluid and protein flux and lung water content was studied in 21 anesthetized dogs. We measured steady-state lung lymph flow, pulmonary arterial and left atrial pressures, and the concentration of total protein and albumin in both lymph and plasma after intratracheal instillation of 2 ml/kg 0.1 N HCl. Acid injury produced a twofold increase in lung lymph flow and lymph protein clearance when compared with control. This indicated an increase in pulmonary microvascular permeability. In dogs given 25 g concentrated human albumin and 1 mg/kg furosemide 10 min after the acid injury, the acid-induced increase in fluid filtration was prevented. However, the decrease in fluid filtration was not attributed to an increase in the transvascular protein osmotic pressure gradient but to a more direct effect of furosemide. Treatment with furosemide alone prevented the increase in lung lymph flow induced by acid injury, whereas albumin alone did not. In all acid-injured animals there was an increase in lung water when compared wtih control. Therefore acid aspiration produced localized areas of damage to filtration vessels that lead to increased leakage of protein and water. Furosemide treatment prevented much of this increased fluid and protein flux by an undefined mechanism.

Albumins↗