vestimИзвестия Национальной академии наук Беларуси. Серия медицинских наукProceedings of the National Academy of Sciences of Belarus, Medical series1814-60232524-2350The Republican Unitary Enterprise Publishing House "Belaruskaya Navuka"10.29235/1814-6023-2018-15-4-391-404vestim-454Research ArticleКЛИНИЧЕСКАЯ И ЭКСПЕРИМЕНТАЛЬНАЯ МЕДИЦИНАCLINICAL AND EXPERIMENTAL MEDICINEГипоксия поджелудочной железы в патогенезе фиброза при хроническом панкреатитеHypoxia of pancreas in pathogenesis of fibrosis in chronic pancreatitishttps://orcid.org/0000-0003-4710-5996ВоробейА. В.VarabeiA. V.

член-корреспондент, д-р мед. наук, профессор, заведующий кафедрой

Corresponding Member, D. Sc. (Med.), Professor, Head of the Department

deptsurg@hotmail.comhttps://orcid.org/0000-0002-4721-7341ШулейкоА. Ч.ShuleikaA. Ch.

канд. мед. наук, доцент

Ph. D. (Med.), Assistant Professor

shuleika1961@gmail.comВладимирскаяТ. Э.VladimirskayT. E.

канд. биол. наук, заведующий отделом

Ph. D. (Biol.), Head of the Department

ШведИ. А.ShvedI. A.

д-р мед. наук, профессор, гл. науч. сотрудник

D. Sc. (Med.), Professor, Chief researcher

ВижинисЕ. И.VizhinisY. I.

канд. мед. наук, доцент

Ph. D. (Med.), Assistant Professor

vigman@mail.ruМаккиМ. Ю.MakkiM. Y.

клинический ординатор

clinical resident

Белорусская медицинская академия последипломного образования, МинскBelarusian Medical Academy of Postgraduate Education, Minsk201814012019154391404Copyright © Воробей А.В., Шулейко А.Ч., Владимирская Т.Э., Швед И.А., Вижинис Е.И., Макки М.Ю., 20192019Воробей А.В., Шулейко А.Ч., Владимирская Т.Э., Швед И.А., Вижинис Е.И., Макки М.Ю.Varabei A.V., Shuleika A.C., Vladimirskay T.E., Shved I.A., Vizhinis Y.I., Makki M.Y.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://vestimed.belnauka.by/jour/article/view/454

Патогенез хронического панкреатита (ХП) и болевого синдрома до конца не изучен. Цель исследования – оценить взаимосвязь фиброзных изменений паренхимы поджелудочной железы (ПЖ), ее гипоксии и панкреатической протоковой гипертензии в патогенезе ХП. В проспективном исследовании проведено морфологическое, иммунногистохимическое изучение препаратов ПЖ, интраоперационно изучены показатели тканевой оксиметрии и панкреатического протокового давления у 40 пациентов, оперированных по поводу ХП. Установлено, что по мере прогрессирования фиброзных изменений в ткани ПЖ пациентов с ХП отмечаются увеличение экспрессии TGF-β1 (р < 0,001), рост количества панкреатических звездчатых клеток (r = 0,32, р < 0,05), снижение содержания гликогена (маркера гипоксии). При интраоперационном прямом измерении наблюдаются высокие показатели внутрипротокового давления: 34,2 (26,6; 45,3) мм рт. ст., снижение оксигенация ткани ПЖ, которые коррелируют со степенью фиброза. Ткани ПЖ при ХП испытывают хроническую гипоксию, связанную с фиброзом и панкреатической протоковой гипертензией. В свою очередь, вторичная ишемия ПЖ может быть значимым фактором в прогрессировании фиброза и хронического болевого синдрома при ХП.

The pathogenesis of chronic pancreatitis and pain syndrome had not been fully studied. The aim of the study was to evaluate the interrelation of fibrotic and ischemic changes in the parenchyma of pancreas, and pancreatic duct pressure in the pathogenesis of chronic pancreatitis. In a prospective study, a morphological, the immunohistochemical study of pancreatic preparations was performed, and the indicators of tissue oximetry and pancreatic duct pressure were studied intraoperatively in 40 patients operated for chronic pancreatitis. It was found that with the progression of fibrotic changes in the pancreatic tissue of patients with chronic pancreatitis, there was an increase in TGF-β1 expression (р < 0.001), an increase in the number of pancreatic stellate cells (r = 0.32, р < 0.05), a decrease in glycogen (ischemia marker). The intraoperative direct measurement revealed a high pancreatic duct pressure: 34.2 (26.6; 45.3) mm Hg, a decrease in oxygenation of the pancreatic tissue that correlate with a degree of fibrosis. The pancreatic tissue in chronic pancreatitis has chronic hypoxia associated with fibrosis and increased pancreatic ductal hypertension. So, secondary pancreatic ischemia can be a significant factor in the progression of fibrosis and chronic pain syndrome in chronic pancreatitis.

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The authors declare that there are no conflicts of interest present.