Email this article Time course of changes in the gastric juice levels of nitric oxide in patients with upper digestive tract diseases
- Authors: Esedov E.M.1, Magomedeminova A.S.1, Esedov EM1, Magomedeminova AS1
-
Affiliations:
- Issue: Vol 82, No 2 (2010)
- Pages: 21-24
- Section: Editorial
- URL: https://ter-arkhiv.ru/0040-3660/article/view/30536
- ID: 30536
Cite item
Full Text
Abstract
Aim. to study the time course of changes in the gastric juice levels of nitric oxide (NO) in patients with esophagogastroduonenal diseases (EGDD).
Subjects and methods. One hundred and seventy-four patients with EGDD were examined.
Results. In patients with chronic atrophic gastritis, the level of NO was significantly lower than the normal levels and correlated with the magnitude of mucosal atrophy. Elevated gastric juice NO levels were noted at exacerbations of gastroesophageal reflux disease (GERD), chronic nonatrophic gastritis (CNAG), and duodenal ulcer disease (DUD). At the end of a therapy course, the gastric juice levels of NO did not achieve the control values in patients with GERD, reduced to the normal values in those with CNAG, although became lower, but remained above the normal values in DUD in a remission phase.
Conclusion. The patients with EGDD were observed to have heterodirectional changes in the content of NO in gastric juice. In the patients with DUD, the remaining gastric juice NO levels above the normal values after ulcerative defect cicatrization are indicative of incomplete reparative processes in the gastric mucosa, i.e. delayed morphological remission. In chronic atrophic gastritis, the gastric juice levels of NO did not achieve normal values after treatment despite the onset of clinical remission which may be caused by a continuous gastric mucosal atrophic process.
Subjects and methods. One hundred and seventy-four patients with EGDD were examined.
Results. In patients with chronic atrophic gastritis, the level of NO was significantly lower than the normal levels and correlated with the magnitude of mucosal atrophy. Elevated gastric juice NO levels were noted at exacerbations of gastroesophageal reflux disease (GERD), chronic nonatrophic gastritis (CNAG), and duodenal ulcer disease (DUD). At the end of a therapy course, the gastric juice levels of NO did not achieve the control values in patients with GERD, reduced to the normal values in those with CNAG, although became lower, but remained above the normal values in DUD in a remission phase.
Conclusion. The patients with EGDD were observed to have heterodirectional changes in the content of NO in gastric juice. In the patients with DUD, the remaining gastric juice NO levels above the normal values after ulcerative defect cicatrization are indicative of incomplete reparative processes in the gastric mucosa, i.e. delayed morphological remission. In chronic atrophic gastritis, the gastric juice levels of NO did not achieve normal values after treatment despite the onset of clinical remission which may be caused by a continuous gastric mucosal atrophic process.
About the authors
Esed Mutagirovich Esedov
Al'bina Serazhudinovna Magomedeminova
E M Esedov
A S Magomedeminova
References
- Видманова Т. А., Шабунина Е. И., Жукова Е. А., Кулик Н. И. Изменение производных оксида азота при язвенной болезни двенадцатиперстной кишки у детей. Рос. педиатр. журн. 2004; 1: 26-29.
- Виноградов Н. А. Многоликая окись азота. Рос. журн. гастроэнтерол., гепатол., колопроктол. 1997; 2: 10.
- Konturek S., Konturek P. Role of nitric oxide in the digestive systems. Digestion. 1995; 56: 1-13.
- Лазебник Л. Б., Дроздов В. Н., Барышников Е. Н. Роль оксида азота (NO) в этиопатогенезе некоторых заболеваний органов пищеварения. Экспер. и клин. гастроэнтерол. 2005; 2: 4-11.
- Аметов А. С., Демидова Т. Ю., Косых С. А. Новые стратегии ангиопротективной терапии у больных сахарным диабетом 2 типа и артериальной гипертензией. Рос. кардиол. журн. 2005; 1: 47-54.
- Манухина Е. Б., Малышев И. Ю., Бувальцев В. И. Эндотелиальная дисфункция и артериальная гипертензия: механизмы и пути коррекции. Кардиоваск. тер. и профилакт. 2003; 2: 26-30.
- Покровский В. И., Виноградов Н. А. Оксид азота, его физиологические и патофизиологические свойства. Тер. арх. 2005; 1: 82-87.
- Chen P., Wu K. Structural elements contribute to the calcium/ almodulin dependence on enzyme activation in human endothelial nitric-oxide synthase. J. Biol. Chem. 2003; 278: 392-400.
- Denninger J., Marietta M. Guanylate cyclase and the NO/ cGMP signaling pathway. Biochim. Biophys. Acta 1999; 1411: 334-350.
- Moncada S., Palmer R. U., Higgs E. A. Nitric oxide: physiology, pathophysiology and pharmacology. Pharmacol. Rev. 1991; 43: 109-142.
- Kubes P. Nitric oxide modulates epithelial permeability in the feline small intestine. Am. J. Physiol. 1992; 262: 1138-1142.
- Маев И. В., Трухманов А. С., Малышев И. Ю., Черемушкина Н. В. Исследование метаболизма оксида азота при гастроэзофагеальной рефлюксной болезни. Клин. перспект. гастроэнтерол., гепатол. 2007; 6: 11-16.
- Руденко С. А. Влияние оксида азота на двигательную и секреторную функции желудка и двенадцатиперстной кишки у больных язвенной болезнью и хроническим гастродуоденитом: Автореф. дис. ... канд. мед. наук. СПб.; 2004. 20 с.
- Саблин О. А., Старосельская Н. А., Стариков В. Н. и др. Некоторые особенности метаболизма оксида азота у больных гастроэзофагеальной рефлюксной болезнью. Экспер. и клин. гастроэнтерол. 2003; 5: 168.
- Голиков П. П., Николаева Н. Ю. Метод определения нитрита/нитрата (NO) в сыворотке крови. Биомедицина. Химия. 2004; 1: 79-85.
- Аруин Л. И. Helicobacter pylori: каким образом один возбудитель вызывает разные болезни. Экспер. и клин. гастроэнтерол. 2004; 1: 36-11.
- Herbay A., Rudi J. Role of apoptosis in gastric epithelial turnover. Microsc. Res. Tech. 2000; 48: 303-311.
- Виноградов Н. А. Антимикробные свойства окиси азота и регуляция ее биосинтеза в макроорганизме. Антибиот. и химиотер. 1998; 43(2): 24-29.
- Nathan C. F., Hibbs J. B. Role of nitric oxide synthesis in macrophage antimicrobial activity. Curr. Opin. Immunol. 1991; 3: 65-70.
Supplementary files
