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Biomedical subjects

J D Reed

Publications and source records attributed to J D Reed.

At least 37 records · Page 2Linked to original sources
PubMed1980

Relationship between hydrogen ion concentration and flow of gastric juice during inhibition of gastric secretion in the cat.

1. The normal relationship between the [H+] and rate of flow of gastric juice was determined in conscious cats prepared with cannulated gastric fistulae. Gastric secretion was monitored during stimulation with pentagastrin, insulin and histamine. 2. [H+] rose asymptotically with the flow of gastric juice. This relationship was quantified by applying the data to the integrated form of the Fick equation for diffusion, a graphical plot of log [H+] vs. 1/flow. The calculated relationships were similar for gastric secretion stimulated by pentagastrin, insulin and histamine, and were used to define the normal relationship between gastric [H+] and flow. 3. Significant inhibition of pentagastrin-stimulated gastric secretion with the histamine H2-receptor antagonists, metiamide and cimetidine, atropine or somatostatin did not alter the normal relationship between [H+] and flow; the [H+] observed fell within the normal range observed at that flow rate in the presence of pentagastrin alone. Similarly, inhibition of insulin-stimulated secretion with metiamide, did not alter the normal relationship between [H+] and flow of gastric juice. 4. These data provide evidence that histamine H2-receptor antagonists, atropine and somatostatin all act to reduce the primary rate of acid secretion and do not influence the [H+] per se, either by interfering with back-diffusion of H+, or by changing the proportions of a non-parietal component of gastric secretion added to the parietal H+ component.

Animals↗
PubMed1980

Gastric acid and pepsin-stimulating activity of non-sulphated fragments of gastrin in the cat.

The gastric acid and pepsin-stimulating activities of several C terminal fragments of non-sulphated human gastrin were investigated in the conscious cat prepared with cannulated gastric fistulae with a reproducible, continuous infusion method to construct dose-response curves. The gastric acid-stimulating activities were quantified by reference to the ED50 and were compared with the activity of synthetic non-sulphated human gastrin 17 (SHG17NS) and cat gastrin 17 (SCG17NS). SHG17NS had an ED50 of 0.329 nmol kg-1 h-1. SHG16NS, SHG15NS and SHG13NS all showed similar activities to SHG17NS. SCG17NS tested at low doses had similar activity to SHG17NS. SHG10NS, G5 and G4 and peptavlon showed progressively lower acid-stimulating activities: 26, 12, 9 and 9%, respectively, compared with SHG17NS. The gastric acid-stimulating activities of all the peptides were paralleled by similar pepsin-stimulating activities. The ratios of pepsin secretion:acid secretion were similar for all the peptides (1--2 microgram pepsin/microEq H+). The results are discussed in relation to the biological activity of the circulating gastrin components in the cat compared with other species and it is argued that component IV (corresponding to gastrin tetradecapeptide or minigastrin) is a major, physiologically active, circulating form of the hormone in the cat.

Animals↗
PubMed1980

Sensitivity of parietal cells to gastrin in the cat: comparison with man and dog.

The ED50 value for exogenous gastrin stimulation of gastric acid secretion in the cat is about 300 pmol kg-1h-1. Comparison with values in man and dog show that the ED50 value for gastrin in man is approximately 6-8 times lower than in cat or dog. The rise in circulating gastrin concentration during infusion of a standard dose of gastrin was 1,340 pg ml-1 in the conscious cat. Comparable studies in man and dog give values of 900 and 300 pg ml-1, respectively. Based on these observations, the sensitivity of the parietal cells to gastrin is in the order man, 1.0; dog, 0.47; and cat, 0.09.

Animals↗
PubMed1979

Effects of a combined oestrogen-progestin preparation on gastric acid and pepsin secretion, serum gastrin concentration and biliary secretion of bile acids, phospholipids, and cholesterol in the cat.

1 Daily ethinyloestradiol (50 mug) and norethisterone acetate (1 mg) treatment (Minovlar) was investigated on gastric acid and pepsin secretion, and fasting serum gastrin concentration in six conscious female cats prepared with chronic gastric fistulae. The effect on biliary secretion of bile acids, phospholipids, and cholesterol was investigated in three conscious female cats prepared with chronic gastric and intestinal fistulae, and cholecystectomy.2 Treatment for 49 days did not alter the gastric acid or pepsin response to either intravenous pentagastrin infusions or a food stimulus. The fasting serum gastrin concentration remained unaltered throughout the study.3 Treatment for 18 days did not alter the percentage concentration of cholesterol in the bile, but reduced the percentage concentration of phospholipid. This was mirrored by a rise in the percentage concentration of bile acids in the bile. These trends were quickly reversed on cessation of treatment.4 There was no sign of cholestasis associated with the treatment. Intestinal flow remained constant throughout the study, there was no lithocholic acid or other abnormal bile acids detectable in any samples, and there was no change in serum aspartate aminotransferase concentration.5 The results suggest that in female cats, treatment with a combined oestrogen-progestin preparation does not exert any beneficial effects on the aetiology of peptic ulceration through the reduction of acid or pepsin secretion, or the lowering of serum gastrin concentration. The preparation shows a tendency to produce more lithogenic bile, and this may partly explain the greater incidence of gall stones in women on the contraceptive pill.

Animals↗
PubMed1979

Endogenous prostaglandins and stimulated gastric secretion in the cat: the effect of various secretory inhibitors.

1. The effects of cimetidine, somatostatin and atropine upon the outputs of acid, pepsin, prostaglandins (PG) E and F in gastric juice secreted in response to i.v. infusions of pentagastrin and histamine (H) have been studied in the conscious gastric fistula cat. 2. At constant rate infusions secretion of PGE occurs and follows a similar pattern to that of gastric acid. However the ratio of H:PGE varies considerably and to an extent inexplicable in terms of assay variation. 3. Inhibition of acid output is matched by inhibition of the output of PGE, but changes in concentration of PGE suggest this is a volume related phenomenon. 4. It is concluded that gastric juice PGE is most unlikely to have a regulatory effect upon acid secretion.

Animals↗
PubMed1978

The effect of anaesthesia on pentagastrin stimulated gastric acid secretion in the cat.

1. The effect of Saffan (alphaxalone and alphadolone acetate) and Nembutal (pentobarbitone) anaesthesia on gastric acid secretion stimulated by I.V. bolus injections of pentagastrin was investigated in the gastric fistula cat. The effect of Saffan anaesthesia was also tested on I.V. near-maximal and sub-maximal infusions of pentagastrin. 2. Neither anaesthetic reduced the acid secreted in response to bolus injections of pentagastrin. Increased acid secretion with the anaesthetic was noted at some doses of pentagastrin in both intact and vagotomized animals. 3. Saffan anaesthesia had no effect on near-maximal gastric acid secretion stimulated by pentagastrin 8 microgram kg-1 hr-1 but increased the response to pentagastrin 1 microgram kg-1 hr-1. 4. It is suggested that the differences in the acid secretory responses of the anaesthetized acutely prepared animal compared with the conscious animal are a consequence of the surgical procedures rather than the state of consciousness.

Alfaxalone Alfadolone Mixture↗
PubMed1978

Characteristics and tachyphylaxis of gastrin-stimulated gastric acid secretion in the cat.

1. The characteristics of gastrin-stimulated gastric acid secretion were investigated in conscious cats fitted with chronic cannulated gastric fistulae, with particular reference to tachyphylaxis. 2. There is a significant postive correlation between the peak acid secretion in response to pentagastrin 8 microgram kg-1 hr-1 and body weight. Male cats secret significantly greater amounts of acid in response to pentagastrin than females. The difference is lessened, but not eliminated, by expressing the acid out put in terms of body weight. 3. Pentagastrin stimulates a dose-dependent increase in acid secretion in the range 0.5-32 microgram kg-1 hr-1 when the response to each dose is assayed on separate occasions. Pentagastrin 64 microgram kg-1 hr-1 does not produce a further increase in acid secretion. The acid response to pentagastrin 1-16 microgram kg-1 hr-1 assayed on a single occasion by a continuous infusion method shows a dose-response relationship up to 8 microgram kg-1 hr-1 when it reaches a plateau of secretion. There is no difference between the two methods of assaying the gastric acid stimulating activity using doses of pentagastrin up to 8 microgram kg-1 hr-1. 4 The acid secretion in response to pentagastrin 8 microgram kg-1 hr-1 reaches a maximum after 45 min of stimulation and thereafter shows tachyphylaxis. Over a period of 5 hr there are at least two phases of tachyphylaxis distinguishable. During the period 0.75--2.5 hr of stimulation there is a fast phase of tachyphylaxis (-32.0 muequivH+kg-1 15 min-1). This is followed by a slow phase of tachyphylaxis (-9.4 muequivH+kg-1 15 min-1) up to 5 hr of stimulation. 5. The absolute rate of the fast phase of tachyphylaxis of acid secretion (muequivH+kg-1 15 min-1) increases with increasing doses of pentagastrin, but rates of tachyphylaxis are similar when expressed as a percentage of the peak acid response to the particular dose of pentagastrin (5.1--7.8% 15 min-1). Synthetic human gastrin-17, the synthetic C-terminal decapeptide of human gastrin and the C-terminal tetrapeptide of gastrin have comparable rates of tachyphylaxis. The possible receptor models for the tachyphylaxis of gastrin-stimulated acid secretion are discussed.

Animals↗
PubMed1978

Structure-activity relationships of eighteen somatostatin analogues on gastric secretion.

1. The effect of somatostatin and eighteen somatostatin analogues on pentagastrin-stimulated gastric acid and pepsin secretion was investigated in the conscious vagotomized cat prepared with chronic gastric fistulae. The majority of the analogues are peptides where D-amino acids are incorporated into the molecule instead of the natural L-isomers. 2. The ID50 for cyclic-somatostatin inhibition of near-maximal gastric acid secretion stimulated by pentagastrin 8 microgram kg-1 hr-1 was found to be 1.29 +/- 0.13 n-mole kg-1 hr-1. Pentagastrin-stimulated pepsin secretion had a lower threshold to somatostatin inhibition than did acid secretion. 3. D-Phe6, D-Phe7, D-Thr10, D-Thr12 and D-Phe6-D-Trp8 analogues all show low biological activity against the secretion of gastric acid and pepsin, growth hormone, insulin and glucagon. None of these analogues are antagonists of the cyclic-somatostatin inhibition of gastric secretion, suggesting that they have low affinity for this somatostatin receptor. 4. The analogues under investigation show parallel changes in activity against gastric and growth hormone secretion, suggesting a similarity between the gastric and growth hormone receptors for somatostatin. 5. D-Cys14 analogues are equipotent with or have a greater potency than cyclic-simatostatin in inhibiting the secretion of gastric acid, growth hormone and glucagon but show low insulin inhibiting activity.

Animals↗
PubMed1978

Exogenous prostaglandins and gastric secretion in the cat.

1. In the conscious gastric fistula cate PGE2 was shown to produce dose-related inhibition of gastric acid and pepsin secreted in response to pentagastrin, histamine and insulin. 2. PGF2alpha had little effect on pentagastrin-stimulated gastric acid and pepsin secretion. 3PGF2 delayed the tachyphylaxis of gastric acid stimulated by pentagastrin and histamine, but not that stimulated by insulin. 4. Although not delaying tachyphylaxis of insulin stimulated acid, PGE2 delayed tachyphylaxis of insulin stimulated pepsin.

Animals↗
PubMed1978

Endogenous prostaglandins and gastric secretion in the cat.

1. The gastric juice outputs of acid, pepsin, PGE and PGF, and the plasma concentrations of PGE and PGF have been measured in response to I.V. infusions of pentagastrin, histamine and insulin in the conscious cat. 2. There were significant correlations between the output of gastric acid and gastric outputs of both PGE and PGF during secretion produced by all stimulants. Furthermore, there were similar significant correlations between the gastric outputs of pepsin and both PGE and PGF. However, during insulin stimulation there was significantly more pepsin output per unit PGE or PGF output than during either pentagastrin or histamine stimulation. 3. The correlations between the outputs of gastric acid and both PGE and PGF were similar during pentagastrin and insulin stimulation whereas those between acid and PGE and PGF altered during the infusion of histamine. 4. It is concluded that these data partially, but not entirely, support the hypothesis that local release of prostaglandins may act as a negative feed-back mechanism on gastric acid secretion. 5. Plasma prostaglandin concentration did not correlate with changes in acid or pepsin secretion.

Animals↗
PubMed1978

Quantitation of somatostatin inhibition of insulin-stimulated gastric acid and pepsin secretion in the cat.

Somatostatin inhibition of gastric acid and pepsin secretion stimulated by insulin-hypoglycaemia was quantified in six conscious cats prepared with cannulated gastric fistulae. Somatostatin 0.5-5 microgram kg-1h-1 produced a dose dependent reduction of both acid and pepsin secretions stimulated by insulin 0.2 u kg-1h-1. The doses of somatostatin which produced 50% inhibition of pepsin and acid secretions (ID50) were not significantly different (0.70 +/- 0.16 and 0.93 +/- 0.11 microgram kg-1h-1 respectively). The slope of the calculated correlation line relating % inhibition of pepsin and % inhibition of acid is within experimental error of unity indicating equality of action of somatostatin on insulin-stimulated acid and pepsin secretion. The results indicate that somatostatin is a more potent inhibitor of insulin 0.2 u kg-1h-1 stimulated acid secretion than pentagastrin 8 microgram kg-1h-1 stimulated acid secretion, but is a more potent inhibitor of pentagastrin--than insulin--stimulated pepsin secretion. As insulin stimulates less acid and more pepsin secretion than pentagastrin, the differences in sensitivities to somatostatin of these secretions produced by the two stimulants is thought to be a result of the different absolute amounts of secretion produced by the stimulants.

Animals↗
PubMed1977

Comparison of the inhibition of histamine- and pentagastrin-stimulated gastric acid secretion by somatostatin in the cat.

The effect of cyclic somatostatin on pentagastrin- and histamine-stimulated gastric acid secretion in conscious cats was studied. Evidence is produced that somatostatin competitively inhibits pentagastrin-stimulated gastric acid secretion whereas it inhibits histamine-stimulated secretion by a mechanism which is not competitive in nature. The vagus nerves seem to be involved in the mode of action of somatostatin as the inhibitory effects are greater in vagotomized than in vagus intact animals.

Animals↗
PubMed1977

Comparison of vagal and meat stimulation on gastric acid secretion and serum gastrin.

The gastric acid secreted per unit of serum gastrin concentration or per unit of gastrin delivered to the gastric mucosa was significantly greater during electrical vagal stimulation than during stimulation by meat extract in the pyloric antrum. There was no significant difference in the concentrations of big, big gastrin or Components I and II in gastric venous serum during the two forms of stimulation. There were significantly greater concentrations of Components II and IV in gastric venous serum during meat extract stimulation than during vagal stimulation. The gastrin in gastric venous serum when meat extract was in the pyloric antrum was comprised of Component IV in addition to Component III whereas gastrin in extracts of cat antral mucosa was predominantly Component III. Gastric acid secretion in response to vagal stimulation was greater than can be accounted for by the action of gastrin alone and cannot be explained by differences in the known gastrin variants in the circulation during the two forms of stimulation.

Animals↗
PubMed1977

The effects of somatostatin and metiamide on tachyphylaxis of pentagastrin stimulated gastric acid and pepsin secretion in the conscious cat.

1. Pentagastrin stimulated gastric acid and pepsin secretions show parallel rates of tachyphylaxis in the conscious cat. The responses to histamine show only slight tachyphylaxis. 2. Somatostatin 10 microng.kg(-1).hr(-1) inhibits pentagastrin but not histamine stimulated acid secretion and inhibits pentagastrin stimulated pepsin secretion. 3. The inhibition of pentagastrin stimulated acid and pepsin secretion by Somatostatin delays the tachyphylaxis of these responses, but the rates of tachyphylaxis when they do subsequently occur are identical. 4. Metiamide 10 mg-kg(-1)-hr(-1) equally inhibits histamine and pentagastrin stimulated acid secretion but does not inhibit pentagastrin stimulated pepsin secretion. 5. Inhibiton of acid secretion during metiamide infusion neither prevents nor delays acid nor pepsin tachyphylaxis. 6. It is suggested that tachyphylaxis of acid and pepsin secretion is a gastrin receptor phenomenon and that Somatostatin occupies or modifies the behaviour of these receptors, preventing tachyphylaxis. Metiamide, however, exerts its action only on the histmine H2-receptor and not the gastrin receptor mechanism, and this apparently does not prevent or delay acid tachyphylaxis.

Animals↗
PubMed1977

Comparison of the effect of somatostatin on gastrointestinal function in the conscious and anaesthetized cat and on the isolated cat pancreas.

1. Somatostatin, 10 microgram kg-1 hr-1, inhibited gastric acid and pepsin secretion stimulated by pentagastrin, 8 microgram kg-1 hr-1, in conscious and anaesthetized cats with chronically implanted gastric fistulae. In the acutely surgically prepared anaesthetized cat, Somatostatin inhibited pepsin secretion but produced little inhibition of gastric acid secretion or mucosal blood flow. 2. Secretin stimulated pancreatic juice volume was not significantly reduced in acutely prepared anaesthetized cats, but there was a limited reduction of cholecystokinin-pancreozymin stimulated pancreatic amylase secretion and gall bladder contraction. 3. Somatostatin had neither stimulatory nor inhibitory effects on electrolyte and amylase secretion in the isolated saline-perfused cat pancreas. 4. The results suggest that some of the effects of Somatostatin may depend on the interaction on the target cell of other factors, nervous or humoral which may vary in different experimental preparations.

Amylases↗