1 Central administration of bombesin inhibits gastric acid production independently of the centrally or peripherally-acting stimuli employed. This study evaluates the role and location of the cerebral nitric oxide (NO) ) in the dorsal motor nucleus of the vagus (DMN). This dose of L-NAME when administered into the nucleus of the tractus solitarious (NTS) did not in¯uence the eects of bombesin. Administration of L-arginine (400 mg kg 71 ) into the DMN restored the acid-inhibitory eect of i.c. bombesin in animals treated with L-NAME. 3 Microinjection of bombesin (12 ng kg 71 ) into the paraventricular nucleus of the hypothalamus (PvN) inhibits acid secretion stimulated by pentagastrin. This inhibitory eect was prevented by a previous injection of L-NAME (80 mg kg 71 ) into the DMN. 4 The release of NO in the DMN following i.c. administration of bombesin was con®rmed by in vivo electrochemical detection. 5 Administration by microdialysis in the DMN of the NO-donor SNAP (25 mM in 1.5 ml min 71 ) into the DMN inhibits pentagastrin-stimulated gastric acid secretion. 6 The present study suggests that nNOS-containing neurons in the DMN have an inhibitory role in the control of gastric acid responses.
Objective: To compare the antimicrobial efficacy and effect on plaque growth of a new silica-based fluoride toothpaste containing 2% zinc citrate/ 0.3% Triclosan with a silica-based fluoride toothpaste containing 0.3% Triclosan/2% copolymer. Methods: In Study 1, plaque was collected after one week's use of each toothpaste and assessed for bacterial viability, live/ dead ratio and microbial membrane integrity. In study 2, plaque was measured immediately and 18 hours after a single brushing with the specified toothpastes. Results: The 2% zinc citrate/0.3% Triclosan formulation significantly reduced the total number of viable aerobic and anaerobic bacteria (p:=0.0223 and p:=0.0443 respectively) compared to the 0.3% Triclosan/2% copolymer formulation. Both toothpastes increased the bacterial membrane permeability significantly. However, the proportion of live bacteria for the 2% zinc citrate/0.3% Triclosan product was significantly reduced (p<0 .05) . Study 2 showed significantly less plaque growth 18 hours after using the 2% zinc citrate/0.3% Triclosan toothpaste compared to the 0.3% Triclosan/2% copolymer toothpaste (p<0.01). Conclusion: Regular use of a fluoride toothpaste containing 2% zinc citrate and 0.3% Triclosan , significantly reduced the viability of plaque bacteria compared to a fluoride toothpaste containing 0.3% Triclosan/ 2% copolymer 12 hours after brushing. In addition, a clinical plaque growth study confirmed that this antimicrobial efficacy leads to a significant reduction in plaque growth.
To study whether renal failure enhances gastric mucosal nitric oxide (NO) formation in the rat, we measured 1) in vivo NO concentration and 2) NO synthase (NOS) activity, content, and mRNA expression in gastric mucosal homogenates of uremic and sham-operated anesthetized rats. Gastric mucosal NO release was measured by an electrochemical technique. NOS content was analyzed by Western immunoblots, using specific monoclonal antibodies. Constitutive (Ca2+ dependent; cNOS) and inducible (Ca2+ independent; iNOS) NOS activities were assayed by following the conversion of L-[U-14C]arginine to [U-14C]citrulline. mRNA expression for the constitutive neuronal (ncNOS), endothelial (ecNOS), and iNOS isoforms was determined by reverse transcription-polymerase chain reaction. Under basal conditions, gastric mucosal NO concentration was significantly greater in uremic compared with control rats. This was accompanied by significantly greater gastric mucosal cNOS activity in uremic rats than in control rats, whereas no differences were observed in iNOS activity between both groups of animals. Moreover, total enzyme content and the levels of gastric mucosal mRNA expression for ncNOS, ecNOS, and iNOS showed no significant differences between uremic and sham-operated rats. These data confirm that, in uremic rats, enhanced Ca2+-dependent NOS activity is responsible for gastric mucosal NO overproduction and suggest that the main regulatory mechanism is not transcriptional but translational and/or posttranslational in nature.
Underlying H. pylori infection aggravates acute NSAID-induced gastric damage. However, at early phases, gastric hyperemia associated with increased nitric oxide production may exert some protective role.
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