Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0847097 (acidity)
 15,165 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In this study, aortic strips taken from mongrel dogs were used as experimental material. After preparation, the aortic strips were incubated in a designed control medium or an experimental medium (adding thrombin or epinephrine to the control medium). The pH value of each incubation medium mentioned above was adjusted with HCl or NaOH to a level of 8.0, 7.4, 7.0 and 6.6, respectively, in order to investigate the influence of medium acidity on the production of endothelin-1 from endothelial cells using aortic strips. After a designated time duration (one hour, three hours, six hours and 12 hours, respectively), the incubation media were collected for assay of endothelin-1. The results demonstrated that the endothelin-1 level of the incubation medium was elevated when: 1) the incubation time was lengthened; 2) the incubation medium was more acidic; 3) the aortic strips were incubated with a stimulant, such as thrombin and epinephrine; and 4) the endothelial cells on the aortic strips were intact. This indicates that the secretion of endothelin-1 is: 1) time-dependent, 2) pH-dependent, 3) stimulant-dependent and 4) endothelium-dependent.
 ...
PMID:Effect of pH on endothelin-1 secretion of aortic strips. 810 71

The role of endogenous sulfhydryls (SH) in the healing of HCl-induced gastric injury was investigated in the rat. The animals fasted for 18 h were given 1 ml of 0.6 N HCl by gavage, and they were fed normally from 1 h later and killed various days after HCl treatment. Gastric lesions induced by HCl healed to quiescent states within 7 days both macroscopically and histologically. Mucosal SH levels were markedly reduced after induction of damage by HCl, but recovered gradually to or above normal values within 5 days. Gastric acidity was also significantly reduced after administration of 0.6 N HCl (induction of lesions), followed by a return to normal values within 5 days, although the volume of gastric contents remained unchanged before and after HCl treatment. The healing of HCl-induced gastric lesions was significantly impaired by diethylmaleate (DEM 0.3 ml/kg x 2) when this drug was given subcutaneously for 5 days. Glutathione (GSH: 100 mg/kg x 2) alone did not affect the healing of gastric lesions, but the combined administration of GSH with DEM significantly antagonized the delayed healing caused by DEM. Administration of DEM caused a marked and persistent reduction in the mucosal SH contents, while GSH by itself significantly increased the mucosal SH levels and partially reversed the reduced SH contents caused by DEM. Gastric acid secretion was not significantly altered by either DEM or GHS. These results suggest that endogenous SH may play some roles in the healing process of gastric mucosal lesions. DEM caused a deleterious effect on the healing of gastric lesions, probably by reducing the mucosal SH.
 ...
PMID:Endogenous sulfhydryls in healing gastric mucosal injury induced by HCl in the rat. 831 44

We adapted a rat model of gastrointestinal candidiasis for studies of in vivo gastric colonization with Candida albicans. Whereas normal rats cleared a single intragastric inoculum of 5 x 10(6) C. albicans from the stomach within 4 hours, rats pretreated with chloramphenicol and gentamicin achieved stable gastric colonization for at least 5 days after administration of this inoculum. We next used this model to study host modifications hypothesized to alter gastric colonization. A first group received dilute HCl 4 hr before yeast inoculation, to induce acute superficial gastric erosions; another group was treated with glucocorticosteroid beginning 12 days before yeast inoculation; and another group received famotidine therapy beginning 3 days before yeast inoculation, to neutralize gastric acidity. Recovery of yeasts from stomachs was significantly different from the control group only in rats treated with steroids; greater colonization was found in the rats so treated. In a final group of experiments, we attempted to inhibit in vivo gastric colonization with yeasts by preincubation of yeasts in vitro with a polyclonal antiserum raised in rabbits against heat-killed C. albicans. We were not able to demonstrate inhibition of gastric colonization by preincubation with this antiserum in this model system.
 ...
PMID:Gastric colonization with Candida albicans. 832 93

The barrier that protects the undamaged gastroduodenal mucosa from autodigestion by gastric juice is a dynamic multicomponent system. The major elements of this barrier are the adherent mucus gel layer, which is percolated by the HCO3- secretion from the underlying epithelial cells; the epithelial layer itself, which provides a permeability barrier and can rapidly repair superficial damage by a process of cell migration referred to as reepithelization or restitution; and a specially adapted vasculature, which provides a supply of HCO3- for transcellular transport and/or diffusion into the mucus layer. Passive diffusion of intestinal HCO3- into the lumen is particularly important when there is superficial damage resulting in increased leakiness of the mucosal epithelium. The process of reepithelization occurs by the migration of performed cells from gastric pits or duodenal crypts. This process is quite distinct from the wound healing and associated inflammatory response that accompany more severe injury or chronic damage. The adherent mucus gel acts as a physical barrier against luminal pepsin and provides a stable unstirred layer that supports surface neutralization of acid by mucosal HCO3-. Surface neutralization by mucosal HCO3- provides a major mechanism of protection against acid in the proximal duodenum. In the stomach, where luminal acidity can fall to around pH 1, other mechanisms of protection must exist, since the surface pH gradient is reported to collapse when luminal H+ exceeds approximately 10 mM. This collapse of the surface pH gradients may reflect, at least in part, that such studies have been mostly performed on non-acid-secreting mucosa where the supply of HCO3- to the interstitium from the parietal cells will be reduced. However, because the gastric mucosa can withstand prolonged exposure to acid without apparent damage, this implies an intrinsic resistance of the epithelial apical surface. This is amply illustrated within the gastric glands that do not secrete mucus and HCO3- yet are exposed to undiluted pepsin and an isotonic solution of HCl. Bicarbonate and mucus secretions together with mucosal blood flow are under paracrine, endocrine, and neural control. The rate of reepithelialization will depend on local chemotactic factors, adhesion mechanisms, and the creation of an acid/pepsin/irritant-free environment under a protective gelatinous or mucoid cap. If optimal conditions are met, then the rate of reepithelialization appears to depend primarily on the intrinsic properties of the migrating cells themselves rather than control by exogenous mediators.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Gastroduodenal mucosal protection. 841 27

The studies were carried out on twenty newborn piglets. They were divided into four groups. The groups no 3 and no 4 were given intragastric 0.18% HCl from the 3th day of experiment. The groups no 2 and no 4 were infected on the 7th day with 10,000 invasive eggs of Ascaris suum. The presence of A. suum larvae in the lungs and liver was examined after one week lasting invasion by Baermann method. The total acidity in the gastric content was measured. The activity of alpha-amylase, lipase and proteases was determined in the extracts from pancreas and in the contents of stomach, duodenum and jejunum. The level of pepsinogens and alpha-amylase in the animals serum was studied. The intensity of Ascaris invasion was slightly higher in the group which was given HCl than in the infected group without HCl. The activity of digestive enzymes in the both groups was similar. Only in the stomach content from the 4th group the activity of pepsin was higher (p < 0.05), and alpha-amylase and lipase were lower (p < 0.01) than in the 2nd and in the 3th group. The level of pepsinogens was always lower and alpha-amylase higher in the serum of infected animals than in uninfected groups.
 ...
PMID:[Effect of Hydrochloric acid on invasion of Ascaris suum; enzyme activity in the digestive system and serum of newborn piglets]. 883 6

The anti-ulcerogenic potential of the aqueous extract of Eremomastax speciosa leaves was investigated using two methods of ulcer induction: HCl/EtOH-induced ulceration and pylorus ligation. With both methods, the extract inhibited gastric ulceration in a dose-related manner. The highest oral dose tested (190 mg/kg) completely inhibited gastric ulceration and significantly reduced gastric acidity compared with the controls. Incubation of gastric juice with the plant extract (190 mg/kg) significantly reduced the acidity of the incubated gastric juice compared with the controls.
 ...
PMID:Eremomastax speciosa: effects of leaf aqueous extract on ulcer formation and gastric secretion in rats. 895 28

The effects of subcutaneous loperamide on gastric lesions induced by necrotizing agents were investigated in the rat. Loperamide produced a dose-dependent increase of gastric fluid volume and inhibition of gastric lesions caused by 0.6 N HCl or absolute ethanol. Pretreatment with naloxone almost completely blocked both fluid pooling effect and mucosal protective effect of loperamide. Omeprazole reduced the acidity of the gastric fluid in rats treated with loperamide without significantly decreasing the fluid volume. Various volumes of acid, given orally immediately before 0.6 N HCl, volume-dependently prevented gastric lesions. We conclude that subcutaneous loperamide protects the gastric mucosa against necrotizing agents through luminal dilution of irritants, which is mediated by naloxone-sensitive opiate receptors.
 ...
PMID:Subcutaneous loperamide prevents gastric lesions induced by necrotizing agents in rats. 944 Jun 36

The thermal inactivation of Salmonella enteritidis phage type 4 and Escherichia coli O157:H7 as affected by temperature (54.5-64.5 degrees C), pH (4.2-9.6 with HCl or NaOH) and NaCl concentration (0.5-8.5% w/w) was studied. Cell suspensions in modified tryptone soya broth were heated in a submerged-coil heating apparatus and survivors were enumerated on tryptone soya agar incubated aerobically. For most thermal inactivation data there was a logarithmic decrease in the viable cell concentration over the initial 4-6 log10 reduction and D-values were fitted. In some cases, tailing of the survivor curves was observed with cells surviving longer than the D-values predicted. Models describing the effect of temperature, pH and NaCl concentration on the thermal inactivation of S. enteritidis and E. coli O157:H7 were produced. For both organisms, predicted z-values of 4.6-7.0 C degrees were obtained depending on conditions, with larger z-values at higher levels of NaCl. Optimum survival occurred between pH 5 and pH 7 and increasing acidity or alkalinity caused a decrease in the predicted D-values. At equivalent pH, acetic acid and lactic acid (at 0.5, 1 and 2% w/w) generally had a similar, or increased, lethal effect compared with HCl, whereas in most cases citric acid had a less lethal effect. For E. coli O157:H7, increasing NaCl concentration had a protective effect up to the maximum tested (8.5% w/w), while for S. enteritidis optimal survival at a NaCl concentration of 5-7% w/w was predicted. The models were validated in foods by comparing predictions with published data. Most (80%) of the predicted D-values from the S. enteritidis model were within the 95% confidence interval (within 2.45-fold of the published data) for different Salmonella serotypes in whole egg, egg albumen, egg yolk, beef and milk. Most (93%) of the predicted D-values from the E. coli O157:H7 model were larger than the limited published data for this organism in meat, poultry, milk and apple juice with 42% within the 95% confidence interval (within 2.05-fold of the published data). The D-value models were incorporated into Version 1, and subsequent versions, of the predictive microbiology software program, Food MicroModel.
 ...
PMID:Development of thermal inactivation models for Salmonella enteritidis and Escherichia coli O157:H7 with temperature, pH and NaCl as controlling factors. 949 35

We have examined the coupling between somatostatin, gastrin, and gastric acidity, using sheep chronically immunized against somatostatin. All immunized sheep had high-titer (3.2 x 10(5) +/- 1.1 x 10(4) M), high-affinity (1.5 x 10(11) +/- 1.2 x 10(10) l/mol) antibodies. However, basal gastrin and gastric acidity were similar to those in control animals, indicating that an inhibitory somatostatin tone was not required for the maintenance of normal basal gastrin and gastric acidity. Omeprazole (a proton pump inhibitor) increased gastric pH to a similar extent in both the control and immunized groups but resulted in a smaller increase in plasma gastrin in the immunized sheep, thus calling into question the assumption that hypergastrinemia associated with hypochlorhydria is the result of somatostatin withdrawal. Pentagastrin- or histamine-stimulated somatostatin secretion reversed or attenuated the omeprazole-induced hypergastrinemia in control but not immunized sheep, demonstrating a functional role for somatostatin and the biological efficacy of the somatostatin immunization. In a separate series of omeprazole-treated sheep, restoration of an acidic gastric pH with intragastric HCl reversed the hypergastrinemia in both control and immunized animals. We conclude that somatostatin is not essential for the acid-mediated regulation of gastrin. The use of a chronically immunized model as opposed to the acute administration of somatostatin antibodies has important advantages in determining the steady-state regulatory role of somatostatin.
 ...
PMID:Active immunization against somatostatin alters regulation of gastrin in response to gastric acid secretagogues. 957 58

In this study, we attempted to confirm the assessment system of incidence of angialgia and thrombophlebitis by evaluating the influence of test solutions on the vascular permeability by intradermal injection into rat skin, and following results were obtained: 1) Dimensions of dye leakage in the rat skin were not increased by injection of one commercially available preparation (solution 1), but increased significantly by injection of a preparation (solution 2) that had induced a high incidence of angialgia in a clinical study. 2) Dimensions of the dye leakage increased significantly by injection of glucose solutions with about four degrees of osmolality ratio. 3) In the injection of acetate buffers with different titratable acidity, dimensions of the dye leakage increased depending on titratable acidity. 4) Solution 1 was adjusted to pH 4.43 with L-lactate, acetic acid of HCl, and then these solutions were intradermally injected to rats. The influence on dimensions of the dye leakage was in the following order of strength: acetic acid >> L-lactate > HCl. These results suggest that the vascular permeability by injection into rat skin is influenced by osmolality, pH, titratable acidity and composition of test solutions. Therefore, this system using the vascular permeability reaction in rat skin may be useful for evaluation of angialgia and thrombophlebitis incidence.
 ...
PMID:[Influence of infusion solution on the vascular permeability in rat skin]. 966 87


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>