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Query: UMLS:C0011570 (depression)
 172,036 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous work has shown blood gastrin levels to be elevated and appetite depressed in ostertagia-infected calves. A possible relationship between raised blood gastrin values and feed intake was investigated in worm-free animals using the human gastric acid secretion inhibitor, omeprazole. An initial dose-titration experiment established that administration of the drug by intravenous injection at 1.95 mg kg-1 (four times the recommended human dose rate) resulted in a marked (5.2-fold) increase in blood gastrin levels in the calf. Daily administration of omeprazole by intravenous injection at 2 mg kg-1 for four days in a subsequent experiment resulted in a significant depression in feed intake (up to 40.4 per cent) which was accompanied by a significant rise in blood gastrin levels (peak 940 pg ml-1; 6.5-fold increase over control values). It is suggested that such a rise in hormone levels would reduce reticuloruminal and abomasal motility, slow down the passage of ingesta and, in turn, lead to a reduction in appetite.
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PMID:Effect of omeprazole treatment on feed intake and blood gastrin and pepsinogen levels in the calf. 270 94

The antrum-fundic section and re-anastomosis (AESR), liberates, in Wistar male rats, genuine antral peptic ulcers. They start within 20 days. They are progressive evolution, penetrating into all gastric walls. Between 7 and 8 months, they involve near organs (spleen, liver, pancreas) and produce a great inflammatory reaction of the peripancreatic ganglions. The antral peptic ulcer is induced if the gastric lesser curvature's nerves are sectioned and a concomitant pyloroplasty is done or not. The gastric hemisection, if anterior or posterior, break out the peptic ulcer only on the same side of the antrum-fundic interruption. In all this situations, except in cases of concomitant pyloroplasty, it is proved a pronounced and significantly increase of the gastric (g/kg), but not pancreatic index. In the AFSR series with nervous section on the lesser curvature and without pyloroplasty, the percentage of antral peptic ulcers in 56%. It is postulated the probably existence, at an antrum-fundic level, of a neuroendocrine center. Its nullification or disturbance by the section and re-anastomosis procedure could generate the antral ulcer and other histologic changes (increase of the "G" cells, hyperplasia of the parietal, ECL and "A like" cells) by one or various hypothetical ways: 1. Direct action, nullifying the normal blocking function of somatostative over the "G" cells and or parietal cells. 2. Disturbing or nullifying the motor pump effect of the gastric antrum, and on this way, enhancing the duodenum-gastric reflux with all know deleterious effects of the bile in the antrum particularly in an acid milieu. 3. Modifying, in the opposite direction, the sensitivity by one hand, of the "G" cells mass and by the other one, of the parietal, ECL and "A like" cells. The depression of the fundic sensitivity will induce the hyperplasia of the "G" cells, the hypersecretion of gastrin and, "a posteriori", all the secretory effects and trophic characteristic of it. 4. Disturbing the prostaglandins secretion, perhaps through a deficit of the nervous innervation, with the resulting epiphenomenon of a cytoprotection deficit mediated through the mucus and bicarbonate production. It is probably that the proposed physiopathogenic mechanism are associated and that the final result, the antral peptic ulcer is the consequence of an increase of the aggressive factors (acid, bile) and a concomitant depression of the defensive factors (cytoprotection), starting normally by the prostaglandins through the mucus and bicarbonate secretion.
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PMID:[Post-sectional antral peptic ulcer and antrofundic re-anastomosis in rats (manifestation of a probable antrofundic neuroendocrine center)]. 306 90

Using adult mongrel dogs, remnant gastric motility in relation to the changes of gastrointestinal hormone (gastrin and motilin) levels were measured under conscious states before and after distal partial gastrectomy in the Billroth I (BI) or II (BII) reconstruction and proximal partial gastrectomy with or without pyloroplasty. Remnant gastric motility was studied during the digestive and interdigestive states by chronically implanted strain gage transducer (S.G.T.) along the gastrointestinal tract. Gastrointestinal hormone levels were determined by radioimmunoassay. Results were summarized as follows: 1. Remnant gastric motility after BI was different from BII, that is, digestive patterns after BII were more shorter than BI, as a result, gastric emptying times were shortened. 2. Gastrin release by the meal intake in the dogs with BI was greater than that in BII. On the other hand, motilin release in the dogs with BII was higher level than that in BI during the digestive and interdigestive states. Gastrointestinal hormone levels after BI were approximately as same responses as controls. These findings suggested that BI reconstruction for distal partial gastrectomy was more physiological surgical procedure than BII reconstruction. 3. Remnant gastric motility during the digestive state after proximal gastrectomy showed the excitatory pattern and gastric emptying time was remarkably shortened than in controls. 4. In gastrin and motilin levels stimulated by the meal in the dogs with proximal gastrectomy, the peak of gastrin and the depression of motilin were observed more early in relation to remnant gastric emptying time. These findings suggested that the pyloroplasty for the proximal gastrectomy was necessary to prevent an increased motility of the remnant stomach during the digestive states.
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PMID:[An experimental study on the remnant gastric motilities and gastrointestinal hormones after various types of gastrectomies]. 324 15

The multisystem involvement in acute pancreatitis (AP) is a reflection of the pancreatic gland's capacity to produce a number of potent vasoactive peptides, hormones, and enzymes. The various prognostic criteria are early evaluations of these metabolic derangements. The pathogenesis of hypocalcemia, long recognized as an indicator of severity of AP, is multifactorial. Imbalances of parathyroid hormone (PTH)-calcitonin, the interactions of glucagon, gastrin and other pancreatic hormones with PTH-calcitonin, the role of free fatty acids in binding serum calcium with albumin, and the translocation of calcium ion in muscles and liver, have been recently described but remain conflicting theories. Yet, the time-honored theory of calcium-soap formation enjoys wide acceptance. Hyperglycemia, hypoglycemia, and occasional ketoacidosis in acute pancreatitis have been studied thoroughly. The complex cause-and-effect relationship between hyperlipidemia with acute pancreatitis needs further study. The coagulation abnormalities seem to be initiated by activated trypsin, and their role in microvascular coagulation appears to form a unifying hypothesis for major organ dysfunction, but this requires further investigation. Adult respiratory distress syndrome may be the result of active enzymes that digest pulmonary surfactant and/or microvascular thrombosis. The depression of cardiac function and shock are suspected to be secondary to vasoactive peptides such as bradykinin, or myocardial depressant factor, whose structure has yet to be elucidated. The renin-angiotensin alterations and renal complications in acute pancreatitis have received scant attention in the literature. The onset of moderate visual disturbances, or even blindness, in a patient with acute pancreatitis as a result of retinal vessel thrombosis is fortunately uncommon. Rare but interesting are the manifestations such as subcutaneous fat necrosis, arthralgia, and pancreatic encephalopathy. Despite the extensive literature on the complexities of the pathogenesis of complications of acute pancreatitis, there have been very few advances in the prevention and management of specific complications. It is hoped that further work on modification of enzymatic disturbances induced in acute pancreatitis will result in its effective treatment and prevention of serious complications.
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PMID:Systemic complications of acute pancreatitis. 328

The inhibition of parotid secretion by pentagastrin increased with dose for jugular and carotid injections (0.01-0.16 micrograms/kg) in acute preparations of 3 sheep anesthetized with sodium pentobarbital. The intracarotid effect exceeded that for the jugular both in magnitude across all doses and in slope relating % inhibition to ln dose (p less than 0.005). The greater depression from carotid injections indicated that the effect was mediated in the head in response to higher pentagastrin concentrations at any dose level. In other experiments, both secretion and associated efferent activity in the parotid nerve were depressed more by carotid than jugular injections of pentagastrin, secretion being reduced by 27.2 vs. 12.1% and efferent activity by 43.2 vs. 20.6% respectively (p less than 0.025). These results indicate that gastrin in the circulation may be able to inhibit parotid secretion in sheep by acting directly on the central nervous system.
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PMID:Parotid secretion and associated efferent activity inhibited by pentagastrin in sheep. 342 11

Strips of muscularis mucosae from the oesophagi of cat, dog and opossum have been studied to determine their responses to drugs to electrical field stimulation. All tissues were contracted by acetylcholine, histamine and, with the exception of strips of muscularis mucosae from the opossum proximal oesophagus, noradrenaline. The effects of acetylcholine and histamine were competitively antagonized by atropine (50 nM) and mepyramine (50 nM) and were abolished by atropine (1 microM) and mepyramine (1 microM) respectively. Contractile responses to noradrenaline were competitively antagonized by phentolamine (50 nM) but were converted to propranolol (50 nM)-sensitive relaxations by phentolamine (1 microM). Relaxations were abolished by propranolol (1 microM). Cholecystokinin octapeptide, gastrin 1 and vasoactive intestinal polypeptide were ineffective on any of the tissues examined. Substance P caused contractions in tissue from all three species. These effects were atropine and tetrodotoxin insensitive. All tissues gave atropine (50 nM)- and tetrodotoxin (100 nM)-sensitive contractions in response to electrical field stimulation. Contractions were not followed by relaxations and spontaneous mechanical activity was not suppressed between periods of stimulation. No evidence was obtained for the presence of non-adrenergic, non-cholinergic inhibitory innervation of the oesophageal muscularis mucosae in any species. During electrical field stimulation noradrenaline always reduced the amplitude of evoked contractions and, with the exception of tissue from proximal opossum oesophagus, increased resting tension. In opossum distal oesophageal muscularis mucosae, the effects of noradrenaline during electrical field stimulation were abolished by a 30 min pretreatment of the tissue with phentolamine (1 microM) and propranolol (1 microM). To Achieve this in all other tissues, it was also necessary to use yohimbine (1 microM). 7 In all tissues where noradrenaline caused a phentolamine (1 microM)-and propranolol (1 microM)- resistant depression of electrically evoked responses, clonidine produced a yohimbine (1 microM)- sensitive depression. 8 Evidence was obtained for the presence of excitatory alpha 1-and inhibitory alpha 2- and beta-adrenoceptors. Inter-species differences in their distribution are discussed.
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PMID:A pharmacological study of oesophageal muscularis mucosae from the cat, dog and American opossum (Didelphis virginiana). 620 83

Vasoactive intestinal polypeptide (VIP), cholecystokinin (CCK) and gastrin in the cerebrospinal fluid (CSF) were studied in patients with endogenous depression, non-endogenous depression, mania, schizophrenia and a control group. All patients were classified according to ICD-9 and the group of depressions was further classified according to the Newcastle Rating Scales for depression (Carney et al. 1965) (N-I). In the group of non-endogenously depressed patients, CSF-VIP levels (median 16 pmol/l) were found to be significantly lower than those of controls (median = 32 pmol/l) and endogenous depressives (36 pmol/l). In the non-endogenous group, it appeared that the low CSF-VIP was due to a group of patients who, during a past or present depressive episode, had been diagnosed as suffering from endogenous depression. Moreover, this group was clinically characterized by 'dysphoric/hysterical features', 'reversed diurnal variation' (i.e. worse in the evening), and 'lack of clearly circumscribed episodes'. In many aspects this group seems similar to the atypical depressives described as monoamine oxidase inhibitor responders. Concerning CSF-CCK and CSF-gastrin, no significant differences between the examined groups were demonstrated.
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PMID:Vasoactive intestinal polypeptide decreased in cerebrospinal fluid (CSF) in atypical depression. Vasoactive intestinal polypeptide, cholecystokinin and gastrin in CSF in psychiatric disorders. 624 Dec 14

The purpose of the present study was to examine the effects of microtubular-microfilament (MT-MF) modifying agents on gastrin release from antral mucosal cells maintained for 3 days under tissue culture conditions. Gastrin levels in the media, determined by radioimmunoassay, were monitored at hourly intervals for 6-8-hr periods. Colchicine, 1 mM, produced mild depression in media gastrin levels and completely inhibited dcAMP-theophylline-induced gastrin release. Ethyl alcohol depressed secretion of gastrin. Conversely, colchicine at 0.01 mM, significantly increased levels of gastrin. Gastrin levels were also significantly increased by tetracaine, 1 mM, and by deuterium oxide, 75% and 37.5%. Cytochalasin D had little effect on resting gastrin levels. Results of these experiments indicate response of gastrin-producing cells maintained under these conditions to a number of test agents; that the secretory responses of gastrin cells to the MT-MF modifying agents are similar to those of other endocrine cells in which concommitant changes in the MT-MF system have been studied, providing support for the proposal that this system is involved in the sequence of intracellular events which leads to gastrin secretion.
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PMID:Studies on gastrin secretion in vitro from cultures of rat pyloric antrum: effects of agents modifying the microtubular-microfilament system. 624 11

The study investigated the relationships between specific demographic, psychosocial, and physiological variables and the severity of duodenal ulcer disease in a population of patients with proved duodenal ulcer. Intercorrelations between psychosocial and physiological variables were also studied. The study design was cross sectional and retrospectively assessed life change units and DUD severity during the previous 6 months in 39 male ulcer clinic outpatients. Anxiety, depression, life change units, the family environment, ABO blood type, secretor status, serum pepsinogen, and serum fasting gastrin were evaluated. A DUD severity score was calculated from self-reported ulcer pain symptoms and ulcer complications. Gastrin levels correlated significantly with three Family Environment Scale (FES) subscales, including: (a) independence, (b) achievement orientation, and (c) expressiveness. Duodenal ulcer disease severity scores correlated with Zung SDS scores, but not with state or trait anxiety, life change units, or the FES.
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PMID:Serum gastrin and the family environment in duodenal ulcer disease. 697 85

Cysteamine in a single subcutaneous administration induces release of gastrin, acid hypersecretion, and duodenal ulcer in rats. Pentagastrin-induced acid hypersecretion has no ulcerogenic effect. The Brunner glands in the proximal duodenum have previously been shown to be an important factor in the natural defence of the duodenal mucosa, and this study has been performed to determine the effect of cysteamine and pentagastrin on the Brunner glands in the rat. The proximal duodenum was isolated in situ and drained by a polyethylene tube. The secretion was studied for two 5-h periods after administration of cysteamine or pentagastrin, and then the Brunner glands were studied histologically. Pentagastrin did not affect spontaneous Brunner gland secretion, whereas cysteamine inhibited the output approximately 50%. After cysteamine the secretory cells were low and depleted of mucus, suggesting that cysteamine interferes with the synthesis of the secretory product. The depression of the Brunner gland secretion may be an important factor in the pathogenesis of cysteamine-induced duodenal ulceration.
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PMID:The effect of cysteamine on the Brunner gland secretion in the rat. 723 83


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