OC.05.3 HOW CAN WE MEASURE ACID SECRETION IN THE SINGLE PATIENT? A VALIDATED NON-INVASIVE SURROGATE TEST COMPARED WITH MAXIMAL ACID OUTPUT IN 600 PEOPLE

The effect of corticosterone and thyroxine on the development of parietal cells was studied in 20-day-old rats. Either corticosterone or thyroxine injection significantly increased the amount of mitochondria, tubulovesicles, and intracellular canaliculi in normal rat pup parietal cells. However, the ultrastructure of parietal cells did not change when rats were adrenalectomized or made hypothyroid by propylthiouracil (PTU) during the first week of life. Corticosterone had the same effect in hypothyroid rats as in normal rats, increasing the volume fraction of mitochondria and the surface density of tubulovesicles and intracellular canaliculi in the parietal cell. However, thyroxine failed to do so in adrenalectomized animals. When 20-day-old adrenalectomized or hypothyroid rats were challenged with secretagogues, there was no increase in maximal acid output over the basal secretory rate, while normal rats showed a 40-50% increase. We conclude that 1) normal parietal cells respond to additional thyroxine or corticosterone with increases in volume fraction of mitochondria and surface density of tubulovesicles and intracellular canaliculi; 2) the dramatic decreases in acid secretion observed in adrenalectomized or PTU-treated rats are not explained by the morphology of parietal cells that remains normal; 3) the effect of thyroxine on the development of acid secretion is mediated by corticosterone; and 4) unlike chief cells the morphological development of parietal cells does not appear to depend on corticosterone or thyroxine after postnatal day 7.

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Gastric acid secretion in Indians with particular reference to the ratio of basal to maximal acid output.

Gut ◽

10.1136/gut.7.6.619 ◽

1966 ◽

Vol 7 (6) ◽

pp. 619-623 ◽

Cited By ~ 18

Author(s):

R K Goyal ◽

P S Gupta ◽

K H Chuttani

Keyword(s):

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Acid Output ◽

Maximal Acid Output

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Spontaneous and Persisting Decrease in Maximal Acid Output

BMJ ◽

10.1136/bmj.2.5757.313 ◽

1971 ◽

Vol 2 (5757) ◽

pp. 313-315 ◽

Cited By ~ 10

Author(s):

H. G. Desai ◽

M. P. Zaveri ◽

F. P. Antia

Keyword(s):

Acid Output ◽

Maximal Acid Output

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Effect of xenopsin on blood flow, hormone release, and acid secretion

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1982.243.3.g195 ◽

1982 ◽

Vol 243 (3) ◽

pp. G195-G199 ◽

Cited By ~ 1

Author(s):

M. J. Zinner ◽

F. Kasher ◽

I. M. Modlin ◽

B. M. Jaffe

Keyword(s):

Blood Flow ◽

Acid Secretion ◽

Gastric Acid ◽

Regional Blood Flow ◽

Acid Output ◽

Significant Inhibition ◽

Organ Blood Flow ◽

Hormone Release ◽

Change In Mean ◽

Specific Influence

We investigated the effects of the neurotensin analogue xenopsin on regional blood flow, central hemodynamics, and stimulated acid secretion in awake conscious dogs. Organ blood flow, estimated using the radioactive microsphere technique, was significantly increased during the xenopsin infusion to the adrenals, pancreas, and ileum. There was no change in mean arterial pressure or cardiac output (measured by thermodilution). Along with changes in blood flow, there was a significant increase in the hormone output from the pancreas. These included rises in plasma pancreatic polypeptide, insulin, and glucagon. There also was a rise in plasma cortisol levels during the infusion. Substance P levels rose slowly but significantly during the xenospin infusion. There was no change in plasma gastrin levels. Xenopsin produced a significant inhibition of tetragastrin-stimulated gastric acid output. Thus, xenopsin appears to have region-specific influence on blood flow that correlates with region-specific hormonal secretion. In addition, xenopsin, like its mammalian analogue neurotensin, is an inhibitor of stimulated gastric acid secretion. A mammalian xenopsinlike peptide may well be involved in the modulation of gastrointestinal function.

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Inhibition of ovine gastric acid secretion by intraduodenal long-chain fatty acids

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1982.243.2.g127 ◽

1982 ◽

Vol 243 (2) ◽

pp. G127-G133

Author(s):

L. M. McLeay ◽

J. M. Fitzgerald

Keyword(s):

Fatty Acids ◽

Fatty Acid ◽

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Unsaturated Fatty Acids ◽

Acid Output ◽

Saturated Fatty Acids ◽

Fatty Acid Content ◽

Conscious Sheep

Effects on ovine gastric function of procedures that increase intestinal unsaturated fatty acid content are unknown, and the present aim was to compare the effects of duodenal unsaturated and saturated fatty acids on gastric secretion in conscious sheep. During the maximal gastric secretory response to a meal, 10 ml gallbladder bile alone or with myristic, palmitic, and stearic acids and oleic, linoleic, and linolenic acids were infused into the duodenum at a rate of 5 g fatty acid . h-1 for 1 h. Compared with control 154 mM NaCl (100%), acid output was reduced to 4-7% of control with infusion of oleic, linoleic, and linolenic acids and myristic acids plus bile. Reductions in acid secretion persisted for up to 5 h from the end of infusion. In contrast, the infusion of palmitic and stearic acids with bile caused mean maximal reductions in acid output, respectively, to only 64 and 55% of control, and levels returned to control within 1 h of the end of infusion. Bile infusion alone caused no reduction in acid secretion. Under the conditions used, C18 unsaturated fatty acids and myristic acid were potent inhibitors of ovine gastric acid secretion. The lesser effects of palmitic and stearic acids were probably related to their reduced solubility and absorption.

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Mechanism of oleic acid-induced inhibition on gastric acid secretion in rats

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1991.260.4.g564 ◽

1991 ◽

Vol 260 (4) ◽

pp. G564-G570 ◽

Cited By ~ 8

Author(s):

J. C. Rhee ◽

T. M. Chang ◽

K. Y. Lee ◽

Y. H. Jo ◽

W. Y. Chey

Keyword(s):

Oleic Acid ◽

Acid Secretion ◽

Peptide Yy ◽

Acid Output ◽

Inhibitory Effect ◽

Rabbit Serum ◽

Similar Degree ◽

Normal Rabbit Serum ◽

Anesthetized Rats ◽

Acid Acid

We investigated the existence of an enterogastrone in rats induced by duodenal administration of oleic acid. Acid secretion by the luminally perfused stomach was stimulated in anesthetized rats by intravenous infusion of 0.3 micrograms.kg-1.h-1 pentagastrin. Intraduodenal administration of 3 mmol of oleic acid produced a profound inhibition (94%) of pentagastrin-stimulated acid output in 10 rats (P less than 0.01). Of several peptides in plasma including secretin, neurotensin, somatostatin, and peptide YY, only secretin was found to increase significantly (P less than 0.001). A similar degree of inhibition of acid output (93%) was caused by porcine secretin, 5.6 pmol.kg-1.h-1, given intravenously to mimic the plasma level of secretin produced by oleic acid infusion. The inhibitory effect of oleic acid on the acid secretion was completely reversed by intravenous injection of a rabbit antisecretin serum but not by a normal rabbit serum. These observations strongly suggest that the inhibition was mediated via circulating secretin. The inhibition produced by either oleic acid or secretin was completely blocked by indomethacin. The blocking action was completely reversed by intravenous administration of 48 micrograms.kg-1.h-1 prostaglandin E2. We conclude that endogenous secretin is a major enterogastrone released by oleic acid in anesthetized rats and that the inhibitory action of secretin requires endogenous prostaglandins.

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Hepatic modulation of insulin-induced gastric acid secretion and EMG activity in rats

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.1980.238.5.r346 ◽

1980 ◽

Vol 238 (5) ◽

pp. R346-R352 ◽

Cited By ~ 2

Author(s):

J. Granneman ◽

M. I. Friedman

Keyword(s):

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Acid Output ◽

Emg Activity ◽

Glucose Levels ◽

Hepatic Portal Vein ◽

Inhibited Acid ◽

Hepatic Portal ◽

The Brain

Intravenous infusions of fructose, a hexose that does not cross the blood-brain barrier, suppressed insulin-induced gastric acid secretion and electromyographic (EMG) activity despite continuing hypoglycemia. Hepatic portal vein infusions of 0.15 M fructose inhibited acid output while the same concentration delivered via the jugular vein did not, suggesting a hepatic site of action of the hexose. Only infusions of fructose that began before onset of the insulin-induced gastric responses were effective, whereas glucose infusions, which elevated plasma glucose levels, readily reversed ongoing gastric activity. The suppressive effects of fructose on gastric activity were prevented by prior section of the hepatic branch of the vagus nerve. In contrast, hepatic vagotomy did not prevent suppression of gastric responses by infusions of glucose, a hexose utilized by both brain and liver. These results suggest that receptors in the brain may initiate and terminate insulin-induced gastric acid secretion and motor activity, whereas sensors in the liver may inhibit these responses.

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Inhibitory effects of beta-adrenergic agonists on gastric acid secretion in dogs

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.1986.251.4.g453 ◽

1986 ◽

Vol 251 (4) ◽

pp. G453-G459

Author(s):

M. H. Stevens ◽

R. C. Thirlby ◽

C. T. Richardson ◽

M. A. Fredrickson ◽

R. H. Unger ◽

...

Keyword(s):

Acid Secretion ◽

Gastric Acid Secretion ◽

Gastric Acid ◽

Intravenous Infusion ◽

Acid Output ◽

Gastric Fistula ◽

Adrenergic Agonists ◽

Inhibitory Effects ◽

Beta Adrenergic ◽

Beta Adrenergic Agonists

We evaluated the effect of two beta-adrenergic agonists, isoproterenol (nonselective agonist) and terbutaline (selective beta 2-agonist), on gastric acid secretion stimulated by intravenous pentagastrin, bethanechol, or histamine in dogs with gastric fistulas. Intravenous infusion of isoproterenol or terbutaline inhibited pentagastrin-stimulated acid secretion to a significantly greater extent than they inhibited bethanechol- or histamine-stimulated acid secretion. For example, isoproterenol (12 micrograms X kg-1 X h-1) reduced mean pentagastrin-, bethanechol-, and histamine-stimulated acid output by 86, 63, and 14%, respectively. Percent inhibition of acid secretion with terbutaline (30 micrograms X kg-1 X h-1) averaged 60, 17, and 24% for pentagastrin, bethanechol, and histamine, respectively. Terbutaline also inhibited pentagastrin-stimulated acid secretion from vagally denervated fundic pouches in a dose-related manner. Plasma somatostatin-like immunoreactivity was significantly higher during infusion of terbutaline plus pentagastrin than during infusion of pentagastrin alone. However, an intravenous infusion of 0.3 microgram X kg-1 X h-1 somatostatin-14 had no effect on pentagastrin-stimulated acid secretion from the gastric fistula, even though this infusion increased plasma somatostatin-like immunoreactivity to the same extent as terbutaline plus pentagastrin infusion. Thus the amount of somatostatin released during terbutaline infusion was not sufficient to explain the inhibition of pentagastrin-stimulated acid secretion observed.

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