Sylastic

Silastic N-nitrosomorpholine.
it was no detected within the esophageal sections of silastic tuve. However , it was detected in the sections exposed to acid gastric when subjects had taken either the control drink or the nitrate drink. The median total N-nitrosomorpholine formed within the silastic tube was 2.3 nmoles on the control day and 4.5 nmoles on the day potassium nitrate wasadministered. On the control day, the peak N-nitrosomorpholine concentration profile was different, producing a plateau rather than the peak concentration recorded without notrate. The N-notrosomorpholine concentration in section 16 was 7.3 mmol/L after nitrate , not much greater than after control drink. The peak N-nitrosomorpholineconcentration after nitrate was measured in section 19,where theconcentration of 8.9 mmol/L was more than 3-fold greater than the 2.7 mmol/L detected in this section of control drink. The one subject in this study who was achlorhydric had no detectable N-nitrosomorpholine in any of the silastic tube sections.
Correlation of silastic tube nitrite versus N-nitrosomorpholine.
The ratio of N.nitrosomorpholine: nitrite within silastic tube is an expression of nitricoxide:nitrite in the lumenof the gastrointestinal tract. N-nitrosomorpholine can be formed only within the epithelial compartment by diffusion of nitric oxide,whereas nitrite can be formed via the diffusion of either nitric oxide or nitrous acid into the tube.
These administration of nitrate resulted in a 3-fold increase in peal silastic tube nitrite concentrations, but only a 50% increased in peakN-nitrosomorpholine: nitrite concentration after nitrate ingestion was .064, wich was significantly lower than .11 after the control drink.
Studies in patients with Barrett?s Esophagus
Eighteen patients were recruited. One patient was unable to tolerate the esophagogastric tube and withdrew from the study. Another patient completed both arms of the sudy.
Gastroesophageal reflux was defined as apH of less than 4 detected 5cm proximal to the clips marking the top of the gastric folds. The pH was less than 4 at this location for a median of 14.5% of 32 study days. On the 16 study day when reflux was stimulated by postural and pharmacologic methods, the pH wass less than 4 at this location for a median of 40% of the study time. This was significantly higer than 3.6%, when reflux was notstimulated wich was in turn significantly higher than 0.1% in the healthy volunteers who received nitrate.
Serum nitrate.
Before administration of the study drink, the median serum nitrate was 11.3mmol/L On the day when reflux was not provoked, wich was not significantly different from 7.8mmo/L on the day we provoked reflux. After administration of 2 mmoles of potassium nitrate, the serumnitrated concentrations increased almost 4-fold on both days, peaking after 60 minutes at 43.1 mmol/L on the day when reflux was not provoked and 37.5 mmol/L on the day we provoked reflux.
Salivary nitrite.
Before the administration of the study drink , the median salivary nitrite concentration was 38.2 mmol/L on the day when reflux was not provoked, wich was not significantly different from 59.2mmol/L on the day we provoked reflux. After administration of 2 mmoles/L of potassium nitrate, salivary nitrate concentrations increased significantly on both days, peaking at 578 mmol/L after 90 minutes on the day when reflux was not provoked an 457 mmol/L after 60 minutes on the day we provoked reflux.
Silastic tube nitrite.
On the day that reflux was stimulated in the patients with Barret´sesophagus, a median of 33% of the total nitrite formed within the silastic tube was formed within the esophageal sections . this was a significantly greater proportion than the median of 8.1% when reflux was not stimulated. In the healthy volunteers who received nitrate, the proportion of nitrite present within the esophagus was 0.7%; wich was insignificantly lower than the Barrett´s esophagus...