Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0038358 (gastric ulcer)
 5,179 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

General pharmacological properties of penfluridol (TLP-607) a long-acting antipsychotic drug, were examined in experimental animals and the following results were obtained. 1) TLP-607 produced a lowering of arterial blood pressure and bradycardia but had almost no effect on respiration and peripheral blood flow. 2) TLP-607 slightly hypertension induced by dopamine, adrenaline and noradrenaline, but had no effect on hypotension induced by acetylcholine and histamine. 3) Antagonistic actions of TLP-607 on such spasmogens as acetylcholine, histamine and barium chloride were slightly stronger than those of haloperidol and chlorpromazine. 4) TLP-607 had neither ganglionic nor neuromuscular blocking action. 5) TLP-607 had a slight or no effect in the following experiments; protection against stomach ulcer, activity of ileum and uterus in vivo and in vitro, urinary volume and electrolytes excretion, and gastro-intestinal propulsion. These results suggest that TLP-607 has no striking peripheral actions in experimental animals.
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PMID:[Pharmacological studies of antipsychotic drug, penfluridol. 2. General pharmacological properties]. 103 5

Catecholamines (adrenaline, dopamine, and noradrenaline) stimulate prostanoid synthesis by acting as "cosubstrates." On the other hand, many inhibitors of leukotriene synthesis, such as nordihydroguaiaretic acid and caffeic acid, have a catecholic structure. Catecholamines have opposite effects on prostanoid and leukotriene synthesis in human polymorphonuclear leukocytes and whole blood. Basic phenols (catechol, hydroquinone, and phenol) also increase the prostanoid/leukotriene ratio in polymorphonuclear leukocytes. These actions correlate to their antioxidant capacities and oxidation potentials, and they are not mediated via adrenergic receptors. There is only limited knowledge about the effects of natural catecholamines on the prostanoid/leukotriene ratio in vitro and in vivo. Indirect data suggest that catecholamines could increase prostanoid production in physiological or pathological situations, such as heavy physical exercise, myocardial infarction, and surgical stress. This interaction may also be of clinical importance in asthma, gastric ulcer, and psoriasis, where decreased prostanoid/leukotriene ratios have been reported.
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PMID:Effects of catecholamines on eicosanoid synthesis with special reference to prostanoid/leukotriene ratio. 145 85

We previously reported that cysteamine induces severe gastric ulcers in WKY, but very mild in SHR. The aim of this study is to elucidate the role on the sympathoadrenal medullary system in the pathogenesis of the cysteamine-induced gastric ulcer. Catecholamine (CA) contents in the stomach and adrenal gland were significantly higher in the non-treated SHR than in the non-treated WKY, suggesting that the sympathetic nervous system is more facilitated in SHR. Cysteamine decreased the noradrenaline and adrenaline contents in these tissues in both strains, however the values of CA was still higher in the treated SHR than the non-treated WKY. Histologically the adrenal medulla was severely damaged by cysteamine administration in WKY than in SHR. In contrast an immunohistological study revealed that chromogranin reactivity of the adrenal medulla was significantly stronger in the treated SHR than in the treated WKY. The celiac plexus was well preserved morphologically even in the cysteamine treatment in both strains. These results suggest that the capacity of the sympathetic nervous system in both the adrenal medulla and the stomach plays an important role in preventing the cysteamine-induced gastric ulcer in SHR.
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PMID:[Inhibition of the cysteamine-induced gastric ulcer by the sympathoadrenal medullary system in spontaneously hypertensive rats (SHR) and normotensive Wistar-Kyoto rats (WKY)]. 175 79

Microinjections of noradrenaline (NA, 0.3, 3.0 and 30.0 micrograms) into the central amygdalar nucleus (CEA) produced dose-related attenuations of cold restraint (3 h at 4 degrees C) induced gastric ulcer formation in rats. On the other hand, stress ulcer aggravating effects were seen with beta-adrenoceptor antagonist, propranolol (10 micrograms) but not with the alpha-adrenoceptor antagonist, prazosin (1 and 10 micrograms). Moderate enhancements of gastric stress lesions were also seen with the NA release inhibitor clonidine (1 microgram) and the neurotoxin DSP-4 (25 micrograms). Further, pretreatment of rats with intra-amygdalar (i.am.) propranolol but not prazosin, antagonized and reversed the gastric cytoprotective effects of NA. The results indicate that beta-adrenoceptor-mediated NAergic mechanisms at the level of the CEA are important for the maintenance of gastric mucosal integrity during immobilization stress.
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PMID:Noradrenergic mechanisms in the central amygdalar nucleus and gastric stress ulcer formation in rats. 232 4

Changes in the contents of various amines and histidine decarboxylase (HDC) activity in the gastric mucosa during the healing process of acetic acid induced gastric ulcer in rats were sequentially examined in the ulcer region and intact region at 2, 10, 40, 80, 180 and 365 days after the operation. The following results were obtained: 1) Histamine (HA) content in the ulcer region was decreased as compared with the intact region at 2 and 10 days and returned to the control level in 40 days. After 180 days, the contents in the ulcer region and intact region were also increased as compared with that of the normal control region. 2) Changes in serotonin (5-HT) content as well as HA content were observed. 3) Norepinephrine content in the ulcer region was decreased as compared with the intact region at 2, 10, 80 and 180 days. 4) HDC activity in the ulcer region was decreased as compared with the intact region at 2, 10 and 40 days, and a lower level was maintained still at 180 days. 5) In the relapse and recurrence of gastric ulcer at 365 days, HA and 5-HT contents in the intact region and ulcer region were not different from those in healing rats, but the contents of these amines were higher at 180 days. The results suggest that the change of HA, 5-HT contents and HDC activity in the gastric mucosa may be one of the factors involved in the relapse and recurrence of chronic ulcers.
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PMID:[Changes in amine contents and regulating enzyme activity of gastric mucosa during the healing process of acetic acid induced ulcer in rats]. 273 3

Methylphenidate (5, 10, or 20 mg/kg/day) or saline were administered to rats in the activity-stress ulcer paradigm. Running-wheel activity and food consumption did not differ among groups. Methylphenidate produced dose-related increases in gastric ulcer severity, decreases in hypothalamic noradrenaline (NA) and increases in 3-methoxy-4-hydroxy-phenylethyleneglycol sulfate (MHPG-SO4) in the hypothalamus, amygdala, hippocampus and thalamus. These results differ markedly from the effects seen with a related substance, d-amphetamine, and suggest different mechanisms of action for these drugs.
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PMID:Methylphenidate effects on activity-stress gastric lesions and regional brain noradrenaline metabolism in rats. 404 33

The spontaneously hypertensive rat (SHR) is a widely used animal model for essential hypertension, and is less susceptible to cold restraint stress in gastric ulcer formation. We previously reported that acid secretion is low in SHR due to sympathetic facilitation compared with normotensive Wistar-Kyoto rats (WKY). The purpose of this study was to evaluate the autonomic nervous function and the gastric mucosal blood flow related to gastric motility during cold restraint stress in SHR. Male SHR and WKY, 24-28 weeks old, were used in this study. Noradrenergic innervation, noradrenaline and dopamine contents in the muscle layer were significantly greater in SHR than in WKY, and tissue choline acetyltransferase activity was significantly lower in SHR. Gastric motility was markedly enhanced by cold restraint stress in WKY. By contrast, SHR maintained the rhythmic and low amplitude contractions regardless of hypothermia. Mucosal blood flow decreased markedly during hypothermia in WKY but was well sustained in SHR. In conclusion, the increase in gastric motility associated with cold restraint stress was suppressed in SHR by sympathetic facilitation in the muscle layer, and this may have contributed to the prevention of ulcer formation by maintaining mucosal blood flow in SHR.
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PMID:Gastric mucosal blood flow in relation to stress-induced hypercontraction in spontaneously hypertensive rats. 776 May 25

Chronic nicotine treatment worsens stomach mucosal damage by cold (4 degrees C) and restraint (stress): it dose- and time-dependently intensifies stress-evoked gastric glandular ulceration, mast cell degranulation and motility. Nicotine 50 micrograms/ml drinking water, given ad libitum to female Sprague-Dawley rats for 10 days, increases the sensitivity of the isolated stomach strip to acetylcholine-induced contractions; atropine abolishes this action. The isolated anococcygeus muscle from nicotine-treated male rats shows increased sensitivity to noradrenaline-induced contractions, but not to those by acetylcholine. Hexamethonium or atropine pretreatment antagonises stress-induced gastric effects in nicotine-drinking rats. Muscarinic M1- and M2-, but not M3-, receptor block (by pirenzepine, AF-DX 116BS and HHSiD, respectively) inhibits stress ulcer formation in female rats. Although tobacco smoking has been reported to increase free radical formation, mucosal xanthine oxidase which initiates free radical formation is uninfluenced by nicotine; antagonising this enzyme (by allopurinol) or hydroxyl free radical scavenging (by dimethylsulfoxide) does not lessen the effect of nicotine on stress-evoked ulceration. The findings suggest that chronic nicotine treatment produces partial ganglionic blockade of the vagal nerve which leads to muscarinic receptor supersensitivity. This phenomenon contributes significantly to the ulcer-worsening mechanism; muscarinic M1- and M2-receptors appear to be involved. The gastric ulcer-aggravating effect of nicotine in stressed rats appears not to be due to increased free radical formation.
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PMID:Nicotine and gastric ulcers in stress. 829 87

The effects of an aggressive biting response on stress-induced noradrenaline (NA) release in the rat amygdala and gastric ulcer formation were studied with an intracerebral microdialysis technique. Rats were exposed to a 60-min period of cold restraint stress with or without being allowed to bite a wooden stick. They were sacrificed 100 min after release from stress to investigate gastric ulcer formation. Cold-restraint stress increased NA release to 304 +/- 22.3 and 206 +/- 23.8% of basal levels (mean +/- SEM) in the nonbiting and biting groups, respectively. The stress-induced increases in NA release in the nonbiting group were significantly higher than those in the biting group. In the nonbiting group, significant increases in NA release continued for 80 min after release from stress; however, NA levels in the biting group recovered to basal levels immediately after the cessation of stress. Although many severe gastric lesions with bleeding were found in the nonbiting group, fewer gastric lesions without bleeding were found in the biting group. The cumulative length of gastric lesions in the nonbiting group and in the biting group was 26.2 +/- 7.4 and 6.8 +/- 3.9 mm (mean +/- SEM), respectively. The mean number of ulcers in the nonbiting group and the biting group was 11.8 +/- 1.3 and 1.8 +/- 0.7 (mean +/- SEM), respectively. Both the cumulative length of ulcers and the number of ulcers were significantly lower than those seen in the nonbiting group. These findings strongly suggest that expression of aggression during stress exposure attenuates not only stress-induced increases in NA release in the rat amygdala but also gastric ulcer formation consequent to stress.
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PMID:Expression of aggression attenuates both stress-induced gastric ulcer formation and increases in noradrenaline release in the rat amygdala assessed by intracerebral microdialysis. 944 32

The gastric mucosa is most susceptible to stress that has been shown to induce mucosal damage in humans and animals. This study aims to explore the underlying mechanisms of partial sleep deprivation, as a source of psychophysiological stress, on gastric functions and its effect on mucosal integrity. Sprague-Dawley rats were partially sleep deprived (PSD) for 7 or 14 days by housing inside slowly rotating drums. Gastric tissues and plasma were sampled at the end of the sleep deprivation periods and mucosal lesion scores were evaluated. Morphological examination was performed after Hematoxylin and Eosin staining. Plasma levels of noradrenaline, adrenaline, gastrin, histamine and somatostatin were determined with enzyme immunoassays. Gastric acidity was measured with acid-base titration in pylorus ligated rats. Gastric mucosal blood flow was evaluated with Laser Doppler Flowmetry. It was found that gastric lesions were induced in about 30%-50% of the PSD rats. Gastric acidity as well as plasma levels of noradrenaline, gastrin and histamine were elevated. Gastric mucosal blood flow and plasma somatostatin level were on the contrary reduced, especially in rats with PSD for 14 days. It is concluded that partial sleep deprivation compromises gastric mucosal integrity by increasing gastric acidity, plasma levels of noradrenaline, gastrin, histamine, and decreasing gastric mucosal blood flow. These results provided experimental evidence on the gastric damaging effects of PSD and it could be one of the risk factors contributing to gastric ulcer formation.
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PMID:Partial sleep deprivation compromises gastric mucosal integrity in rats. 1586 6


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