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1.
Am J Physiol Cell Physiol ; 281(2): C430-8, 2001 Aug.
Article in English | MEDLINE | ID: mdl-11443042

ABSTRACT

Rapid epithelial repair (restitution) after injury is required to maintain barrier function of the gastrointestinal mucosa and skin and is thought to be a highly ATP-dependent process that would be inhibited under hypoxic conditions. However, little is known about the metabolic pathways required for restitution. Thus, this study was undertaken to evaluate, in vitro, the role of oxidative respiration and glycolysis in restitution after injury. To this end, restitution of the bullfrog gastric mucosa was evaluated under the following conditions: 1) blockade of mitochondrial respiration; 2) blockade of glycolysis; or 3) absence of glucose. The extent of mucosal repair after injury was evaluated by electrophysiology and morphology. Cell migration, repolarization, and the formation of tight junctions after injury occurred during blockade of mitochondrial respiration, whereas the recovery of mucosal barrier function did not. In contrast, glycolytic inhibition completely blocked all aspects of restitution by inhibiting the migration of surface epithelial cells. Restitution occurred in tissues incubated with glucose-free solutions, suggesting that cells contain sufficient glucose (glycogen) to drive glycolysis for many hours. Our results demonstrate that the glycolytic pathway is essential for restitution after injury in the bullfrog gastric mucosa and that all but complete repair of barrier function occurs in the absence of mitochondrial respiration.


Subject(s)
Energy Metabolism/physiology , Gastric Mucosa/injuries , Gastric Mucosa/physiopathology , Wound Healing/physiology , Wounds and Injuries/physiopathology , Animals , Cell Movement/drug effects , Deoxyglucose/pharmacology , Gastric Acid/metabolism , Gastric Mucosa/pathology , Glycolysis/drug effects , Iodoacetic Acid/pharmacology , Potassium Cyanide/pharmacology , Pyruvic Acid/pharmacology , Rana catesbeiana , Reference Values , Sodium Azide/pharmacology , Wounds and Injuries/pathology
2.
Am J Physiol Gastrointest Liver Physiol ; 279(2): G400-10, 2000 Aug.
Article in English | MEDLINE | ID: mdl-10915650

ABSTRACT

This study was undertaken to determine the mechanism by which ammonium chloride (NH(4)Cl) inhibits stimulated acid secretion in the bullfrog gastric mucosa. To this end, four possible pathways of inhibition were studied: 1) blockade of basolateral K(+) channel, 2) blockade of ion transport activity, 3) neutralization of secreted H(+) in the luminal solution, or 4) ATP depletion. Addition of nutrient 10 mM NH(4)Cl (calculated NH(3) concentration = 92.5 microM and NH(4)(+) concentration = 9.91 mM) inhibited acid secretion within 30 min. Inhibition of acid secretion did not occur by blockade of basolateral K(+) channel activity or ion transport activity or by neutralization of the luminal solution. Although ATP depletion occurred in the presence of NH(4)Cl, the magnitude of ATP depletion in 30 min was not sufficient to inhibit stimulated acid secretion. By comparing the effect of NH(4)Cl on the resistance of inhibited or stimulated tissues, we demonstrate that NH(4)Cl acts specifically on stimulated tissues. We propose that NH(4)Cl blocks activity of an apical K(+) channel present in stimulated oxyntic cells. Our data suggest that the activity of this channel is important for the regulation of acid secretion in bullfrog oxyntic cells.


Subject(s)
Ammonium Chloride/pharmacology , Hydrochloric Acid/metabolism , Parietal Cells, Gastric/metabolism , Potassium Channels/physiology , 4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid/pharmacology , Adenosine Triphosphate/metabolism , Ammonia/metabolism , Animals , Barium/pharmacology , Biological Transport/drug effects , Biological Transport/physiology , Bumetanide/pharmacology , Carbachol/pharmacology , Carbon Radioisotopes , Cholinergic Agents/pharmacology , Cimetidine/pharmacology , Clotrimazole/pharmacology , Diuretics/pharmacology , Enzyme Inhibitors/pharmacology , Gastric Mucosa/cytology , Gastric Mucosa/drug effects , Gastric Mucosa/metabolism , Growth Inhibitors/pharmacology , Histamine/pharmacology , Hypoglycemic Agents/pharmacology , Imidazoles/pharmacology , Methylamines/pharmacology , Microscopy, Electron , Omeprazole/pharmacology , Ouabain/pharmacology , Parietal Cells, Gastric/drug effects , Parietal Cells, Gastric/ultrastructure , Potassium Channel Blockers , Protons , Rana catesbeiana , Tetraethylammonium/pharmacology , Tolbutamide/pharmacology
3.
J Endod ; 18(2): 63-7, 1992 Feb.
Article in English | MEDLINE | ID: mdl-19186420

ABSTRACT

Adsorption of some paraformaldehyde was noted in a previous study evaluating its sterilizing effect on gutta-percha (GP). This study examined histologically the effect of this adsorption when formaldehyde-exposed GP was implanted into the subcutaneous connective tissue of rats. GP implants were prepared in cylinder shape using a template designed to standardize size. Fifty GP cylinders were exposed to paraformaldehyde for 7 days before being implanted, while 50 others were implanted without exposure. Fifty rats had two implant sites prepared, at dorsal-interscapular and dorsal-caudal regions. Sham operations were performed on 10 rats to examine the effect of the surgery itself. The animals were killed at 4, 7, 14, 28, and 56 days. There was a significant difference between the two categories of implants only at 7 days, with the GP specimens without paraformaldehyde exposure showing more inflammation than GP with paraformaldehyde specimens (p = 0.043). Although the GP-alone specimens showed greater initial inflammation, both groups recovered in the same time period. One of the GP specimens with paraformaldehyde still showed a moderate/severe response at 56 days, whereas all of the GP-alone specimens showed only none/mild responses. The GP examined appeared to cause more inflammation than was expected.


Subject(s)
Anti-Infective Agents, Local/toxicity , Formaldehyde/toxicity , Gutta-Percha/toxicity , Polymers/toxicity , Root Canal Filling Materials/toxicity , Subcutaneous Tissue/drug effects , Animals , Cellulitis/chemically induced , Cellulitis/pathology , Fibroblasts/pathology , Lymphocytes/pathology , Macrophages/pathology , Models, Animal , Neutrophils/pathology , Plasma Cells/pathology , Rats , Rats, Sprague-Dawley , Subcutaneous Tissue/pathology , Time Factors
4.
J Endod ; 15(9): 427-31, 1989 Sep.
Article in English | MEDLINE | ID: mdl-2637336

ABSTRACT

The effects of steam sterilization and usage on sharpness were evaluated on #25 endodontic files. Files were used to instrument 1, 5, and 10 molars. Control groups determined the effect of steam sterilization alone on cutting efficiency of unused files. A cutting efficiency test was performed on an apparatus that compares sharpness of files when used in linear motion. Scanning electron microscopic analysis was performed in each group. Significant differences were found between experimental files used to instrument 1 molar and those used for 5 or 10 molars. The difference in cutting efficiency between the second and third experimental groups was not significant, indicating that most of the decrease in sharpness occurred with use between one and five molars. No significant difference was found between the control groups, indicating no decrease in cutting efficiency by sterilization alone. The scanning electron microscopic analysis supported the statistical data.


Subject(s)
Dental Instruments , Steam/adverse effects , Sterilization/methods
6.
Gen Dent ; 34(3): 238-40, 1986.
Article in English | MEDLINE | ID: mdl-3459692
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