The intestinal transport of D-xylose was studied during the acute poisoning of male Wistar rats with orally administered potassium nitrate and sodium nitrite. At the peak of xylose absorption, the metabolic parameters of Na+/K(+)-ATPase, alkaline phosphatase, oxygen uptake, and lactic acid level were determined in the small intestine mucosa. Nitrite in a dose of 80 mg NaNO2/kg b.w. increased the permeability of gastric mucosa for D-xylose and raised the uptake of oxygen by the small intestine mucosa. No changes were observed in the activity of Na+/K(+)-ATPase and alkaline phosphatase. A dose of 10 mg NaNO2/kg b.w. was not followed by increased absorption of this sugar. It was also demonstrated that potassium nitrate had no effect on the process of intestinal absorption of D-xylose and failed to change the determined metabolic parameters of the small intestine mucosa.
The intestinal transport of D-xylose was studied during subchronic poisoning of male Wistar rats with the oral administration of potassium nitrate and sodium nitrite. The metabolic parameters of small intestine mucosa were determined one hour after xylose administration, i.e., Na+/K(+)-ATPase, alkaline phosphatase, oxygen consumption, and lactic acid level. Nitrite reduced the absorption of xylose and decreased the activity of Na+/K(+)-ATPase and alkaline phosphatase. No effect of sodium nitrite was demonstrated on the aerobic metabolism of intestinal mucosa with an increased lactic acid level. Potassium nitrate did not effect the processes of intestinal absorption of xylose nor the metabolic parameters of small intestine mucosa.
The intestinal absorption of D-xylose was studied during acute poisoning of male Wistar rats receiving intragastrically potassium nitrate and sodium nitrite and small intestine perfusion with these compounds. The metabolic parameters, Na+/K(+)-ATPase, alkaline phosphatase, oxygen uptake, and lactic acid level, were assessed in the small intestine mucosa one hour after administration of these compounds. Exercise was demonstrated to reduce the intestinal absorption of D-xylose, to raise the level of lactic acid, and to increase the oxygen uptake by the small intestine mucosa, but caused no changes in the activity of Na+/K(+)-ATPase or alkaline phosphatase. Also, exercise failed to change the direction of the toxic effects of sodium nitrite but increased potassium nitrate toxicity as evidenced by reduced absorption of D-xylose from the intestine despite lack of changes of the enzymes Na+/K(+)-ATPase and alkaline phosphatase in the mucosa.
The intestinal absorption of D-xylose was studied during the subchronic poisoning of male Wistar rats with orally administered potassium nitrate and sodium nitrite associated with exercise; running on a moving track during the last two weeks of poisoning. The metabolic parameters of Na+/K(+)-ATPase, alkaline phosphatase, oxygen uptake, and lactic acid level in the small intestine mucosa were determined one hour after D-xylose treatment. Exercise increased the toxicity of potassium nitrate and sodium nitrite. The experiment demonstrated post-exercise reduction of D-xylose absorption and decrease activity of Na+/K(+)-ATPase and alkaline phosphatase. Exercise caused transient hypoxia of the small intestine, which was observed only in the groups subjected to exercise on the day of the determinations.
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