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Biomedical subjects

J D Reed

Publications and source records attributed to J D Reed.

At least 55 records · Page 3Linked to original sources
PubMed1976

The effect of metramide on the prolonged serum gastrin response to feeding observed in patients with duodenal ulcer.

The response of serum gastrin to a meal has been studied in 11 normal subjects and 16 patients with duodenal ulceration. The mean serum gastrin concentration rises after a meal to similar peak values in both normal subjects and duodenal ulcer patients, and fall to basal values with 3 hours in normal subjects. In duodenal ulcer patients the peak concentration is sustained throughout the 3 hour test period, and this response is not affected by the administration of Metiamide. It is concluded that the control of gastrin release is defective in duodenal ulceration, and this may be due to a failure of the antral pH feedback mechanism. Gastrin may be a primary pathogenetic factor in duodenal ulceration.

Adult↗
PubMed1976

Bromocriptine potentiation of gastric acid secretion in cats.

Bromocriptine administered both orally and intravenously potentiated gastric acid secretion in response to submaximal pentagastrin stimulation in cats. Bromocriptine did not increase the maximum acid secretion in response to pentastrin, not did it stimulate basal acid secretion. Potentiation was observed in normal and vagotomized animals which precludes involvement of the vagi in the response. The mechanism of action of this compound on the stomach does not appear to be mediated through stimulation of dopaminergic receptors as no potentiation was observed with dopamine infusions. It is argued that the bromocriptine potentiation of gastric acid secretion may be a demonstration of 5-hydroxytryptamine or alpha-adrenergic antagonism. However, the potentiation observed with daily oral bromocriptine treatment had disappeared by the eighth day and may correlate with the disappearance of gastric side effects noted in patients on bromocriptine treatment.

Animals↗
PubMed1976

Effects of isopropylnoradrenaline on tachyphylaxis of gastrin stimulated gastric acid secretion and mucosal blood flow in the anaesthetized cat.

1. Gastric acid and mucosal blood flow responses to sustained gastrin stimulation were studied in anaesthetized cats. 2. Acid and mucosal blood flow showed identical rates of tachyphylaxis to both large (maximal) and small doses of gastrin. 3. Isopropylnoradrenaline infused either intravenously or close arterially to the stomach produced increases in blood flow unrelated to time following the peak response to large doses of gastrin, whereas increases in acid secretion appeared to be a part removal of the acid tachyphylaxis. 4. During stimulation by small doses of gastrin, isopropylnoradrenaline increased both blood flow and acid secretion above the peak responses to gastrin alone. 5. Increases in gastrin stimulated acid and mucosal blood flow were also produced by expansion of the blood volume by dextran-saline infusions. 6. The physiological significance of these findings is discussed. 7. It is concluded that tachyphylaxis of gastric acid secretion to gastrin may be a function of the primary tachyphylaxis of mucosal blood flow.

Animals↗
PubMed1976

Pepsin secretion in the anaesthetized cat and the effect of sympathetic nerve stimulation.

1. Experiments were performed on chloralose anaesthetized cats and gastric mucosal blood flow, acid and pepsin secretions were measured. Gastric mucosal pepsin and protein contents were measured at the end of the experiments which were done in three groups: gastrin (A), vagal (B), vagal and sympathetic nerve (C) stimulations. 2. Vagal stimulation significantly reduced (76%) the pepsin content of gastric mucosa compared with gastrin stimulated animals, none of which secreted pepsin. 3. The sum of the secreted and extracted pepsins for all the three groups was not significantly different. There was no significant difference in the extracted protein from any of the groups. 4. Gastric mucosal blood flow, acid and pepsin outputs all had significant correlations with time during the first 70 min of vagal stimulation. During the period 80-160 min of vagal stimulation acid secretion and mucosal blood flow were not correlated with time but pepsin output declined significantly. From 170 to 220 min of vagal stimulation, acid and pepsin outputs and mucosal blood flow were not correlated with time. 5. The assumed pepsin store during each period was calculated and after 40 min of vagal stimulation there is a constant percentage pepsin output from this assumed store. 6. There is some data to suggest that pepsinogen synthesis was occurring during the period 170-220 min of vagal stimulation. 7. Sympathetic nerve stimulation which started at 160 min after the beginning of sustained vagal stimulation, significantly inhibited gastric acid secretion and mucosal blood flow, and in addition it significantly inhibited pepsin secretion. This is consistent with the hypothesis that sympathetic nerve inhibition of gastric mucosal function is mediated by a vasoconstrictor mechanism.

Animals↗
PubMed1975

Direct inhibition of gastric acid and pepsin secretion by growth-hormone release-inhibiting hormone in cats.

Growth-hormone release-inhibiting hormone (G.H.-R.I.H.) inhibited gastric acid and pepsin secretion in response to pentagastrin and food stimulation in cats. This effect is mediated by a direct action on the parietal and peptic cells. No evidence of a post-inhibitory acid or pepsin secretory rebound was obtained. Thus a compound of hypothalamic origin can exert a direct effect on exocrine secretion. In view of its widespread actions and its presence in relatively high concentrations in various organs apart from the hypothalamus, G.H.-R.I.H. might also be regarded as a factor responsible for local coordination of endocrine and exocrine secretion.

Animal Feed↗
PubMed1975

Early clinical experience with metiamide, a histamine H2-receptor antagonist, in patients with duodenal ulcer.

The clinical, endoscopic, and biochemical effects of metiamide, a histamine H2-receptor antagonist, in therapeutic dosage have been studied in a 28-day open trial in patients with duodenal ulcer disease. A good symptomatic response, combined with a 72% ulcer healing rate was observed. There were small but significant rises in plasma creatinine, serum glutamic oxaloacetic transaminase, and serum lactate dehydrogenase during treatment. Small quantities of amino acids appeared in the urine, and the heart size increased slightly. It is concluded that histamine H2-receptor antagonism may be an important therapeutic approach to duodenal ulcer disease.

Adult↗
PubMed1975

Does histamine have two vasodilator actions on the gastric mucosa?

It has been shown previously that there is a greater gastric mucosal blood flow response to histamine than to gastrin stimulation for similar acid secretory values. We have confirmed these observations under steady state conditions and also shown that the oxygen consumption depends on acid secretion in a similar way for both histamine and gastrin stimulation. Furthermore the degree of oxygen extraction from the gastric circulation is significantly less (p less than 0.001) during histamine stimulation than during gastrin stimulation. This supports the hypothesis that histamine causes a vasodilatation in the gastric mucosa in two ways, one may be linked to secretory activity and the other a pure dilator action.

Animals↗
PubMed1975

The mechanism whereby growth hormone-release inhibiting hormone (somatostatin) inhibits food stimulated gastric acid secretion in the cat.

Growth hormone-release inhibiting hormone (somatostatin) inhibits the gastric acid response to food in concious cats. We have confirmed that this tetradecapeptide blocks the food stimulated gastrin release. However, the inhibition of gastrin release is delayed relative to that of acid secretion, &howing that the inhibition of food stimulated acid secretion is by primary effect on the acid secretory mechanism. No evidence was found of potentiation of either the gastric acid output or serum concentration of gastric in response to food.

Animals↗
PubMed1975

Variation in the proportions of individual pepsins secreted by the cat in response to vagal stimulation and hypoglycaemia.

1. Gastric juice was collected at regular intervals during electrical stimulation of the vagus in anaesthetized cats and during insulin hypoglycaemia in both anaesthetized and conscious cats. The total amounts of acid and pepsin secreted were similar in the three groups. 2. Pepsins were examined by agar-gel electrophoresis. Resting juice contained two pepsins, and up to nine pepsins could be detected after stimulation. Three patterns of pepsin secretion were found. 3. The most noticeable feature was the variation in the proportion of total pepsin attributable to the pepsin which migrated most rapidly during electrophoresis (pepsin 1). In response to insulin hypoglycaemia, anaesthetized cats secreted only a small proportion of total pepsin 1 and conscious cats secreted a large proportion as pepsin 1. During direct electrical stimulation of the vagus, the proportion of pepsin 1 rose. 4. The possibility of a dependence of pepsin 1 secretion on vagal stimulation is discussed and the relevance of this to peptic ulcer and to vagotomy is considered.

Animals↗
PubMed1975

The effects of burimamide and metiamide on basal gastric function in the cat.

1 Burimamide injected intravenously in the anaesthetized or conscious cat produced significant increases in gastric acid secretion: in the anaesthetized cat it produced increased gastric mucosal blood flow. 2 Metiamide, in doses which inhibited pentagastrin-stimulated acid secretion, produced no increase in gastric acid secretion in conscious animals, or gastric acid secretion or gastric mucosal blood flow in the anaesthetized cat. 3 Metiamide did not influence the amount of acid which diffused out of the stomach when instilled at pH values between 1.5 and 6.0. 4 The possible mode of action of burimamide in increasing basal gastric secretion is discussed.

Anesthesia↗
PubMed1975

The effect of sympathetic nerve stimulation on acid secretion, regional blood flows and oxygen usage by stomachs of anaesthetized cats.

1. Gastric acid secretion, and total gastric and mucosal blood flows (amidopyrine technique) were measured in anaesthetized cats. Oxygen contents of arterial and gastric venous blood were measured using an oximeter. 2. Splanchnic nerve stimulation (10 Hz) significantly reduced the acid output and total gastric and mucosal blood flows produced in response to maximal gastrin pentapeptide infusions. 3. The arterial haemoglobin concentration was significantly reduced during splanchnic nerve stimulation, and this is consistent with the hypothesis that the splanchnic nerve effect is directed against precapillary sphincters. 4. During the period of inhibition, gastric oxygen consumption and acid secretion were reduced to similar degrees. There was no significant change in oxygen extraction by the stomach. 5. It remains possible that the splanchnic nerves directly inhibit the parietal cell activity.

Animals↗
PubMed1975

The effect of sympathetic nerve stimulation on serum gastrin, gastric acid secretion and mucosal blood flow responses to meat extract stimulation in anaesthetized cats.

Chloralose anaesthetized cats were prepared with fundic and antral pouches. Fundic mucosal blood flow was measured by the amidopyrine technique and serum gastrin was measured by radioimmunoassay. 2. Meat extract suspension in the pyloric antrum produced a highly significant sixfold increase in arterial serum gastrin concentration (P less than 0-001). 3. The mean ratio of the fundic mucosal blood flow to acid secretory responses (deltaMBF/deltaH+ ratio) of 0-142 +/- 0-026 (25) ml./muequiv H+, is very similar to the values previously published for exogenous gastrin stimulation. 4. Splanchnic nerve stimulation, during responses to meat extract stimulation, produced significant reductions in gastric acid secretion (P less than 0-025), fundic mucosal blood flow (P less than 0-02), Arterial serum gastrin concentration (P less than 0-01) And gastrin delivered to the mucosa (P less than 0-001). 5. In the 30 min period following the end of splanchnic nerve stimulation only arterial serum gastrin concentration remained significantly reduced.

Animals↗
PubMed1975

Gastrin response to meals of different composition in normal subjects.

The serum gastrin responses and the integrated gastrin responses to eating three meals of very different composition were studied in the same normal subjects on different days. Two meals, a milk meal of 500 ml, and a breakfast of eggs, toast, butter, marmalade, fruit juice and coffee, were eaten at breakfast time. The serum gastrin responses to these meals were compared and contrasted with the concentrations observed when the subjects fasted over the same time of day. A steak meal was eaten at lunch time. There were no significant differences between the mean serum gastrin concentrations to the three meals but each meal produced a significant increase in serum gastrin above fasting levels. When the prefeeding gastrin concentration was subtracted from the gastrin responses then the integrated responses to the steak meal were greater than those to either of the breakfast meals. Considerable variability in response to any one meal was observed within the group of subjects, but those subjects who produced high serum gastrin concentrations to one meal did so to the others. Conversely, at low response to one meal was reflected in low responses to the other two meals. Fasting serum gastrin concentration was correlated with the age of the subject. Repeatability of the response to one meal was tested in two subjects who ate the same meal on four separate occasions showing their responses to be repeatable.

Adult↗