cfpdБюллетень физиологии и патологии дыханияBulletin Physiology and Pathology of Respiration1998-5029Дальневосточный научный центр физиологии и патологии дыхания10.36604/1998-5029-2020-76-118-125cfpd-808Research ArticleОБЗОРЫREVIEWSНейрогенная дисфункция дыхательной системы при черепно-мозговой травмеNeurogenic dysfunction of the respiratory system in traumatic brain injuryЗиновьевС. В.ZinovievS. V.

Сергей Викторович Зиновьев - кандидат медицинских наук, старший научный сотрудник, Центральная научно-исследовательская лаборатория.

690002, Владивосток, пр-т Острякова, 2

Sergey V. Zinoviev - PhD (Med.), Senior Staff Scientist, Central Research Laboratory.

2 Ostryakova Ave., Vladivostok, 690002

sinowev@mail.ruПлеховаН. Г.PlekhovaN. G.

Наталья Геннадьевна Плехова -  доктор биологических наук, заведующая Центральной научно-исследовательской лабораторией.

690002, Владивосток, пр-т Острякова, 2

Natalia G. Plekhova - PhD, D.Sc. (Biol.), Head of the Central Research Laboratory.

2 Ostryakova Ave., Vladivostok, 690002

pl_nat@hotmail.comРадьковИ. В.RadkovI. V.

Иван Валерьевич Радьков - аспирант, Центральная научно-исследовательская лаборатория.

690002, Владивосток, пр-т Острякова, 2

Ivan V. Radkov - Postgraduate student, Central Research Laboratory.

2 Ostryakova Ave., Vladivostok, 690002

radiarest@gmail.comШуматовВ. Б.ShumatovV. B.

Валентин Борисович Шуматов - доктор медицинских наук, профессор, ректор.

690002, Владивосток, пр-т Острякова, 2

Valentin B. Shumatov - MD, PhD, D.Sc. (Med.), Professor, Rector.

2 Ostryakova Ave., Vladivostok, 690002

mail@tgmu.ruФедеральное государственное бюджетное образовательное учреждение высшего образования «Тихоокеанский государственный медицинский университет» Министерства здравоохранения Российской ФедерацииPacific State Medical University202026062020076118125Copyright © Зиновьев С.В., Плехова Н.Г., Радьков И.В., Шуматов В.Б., 20202020Зиновьев С.В., Плехова Н.Г., Радьков И.В., Шуматов В.Б.Zinoviev S.V., Plekhova N.G., Radkov I.V., Shumatov V.B.Данная работа распространяется под лицензией Creative Commons Attribution 4.0.This work is licensed under a Creative Commons Attribution 4.0 License.https://cfpd.elpub.ru/jour/article/view/808

Развитие дыхательной недостаточности при черепно-мозговой травме (ЧМТ) связано с возникновением некардиогенного, нейрогенного отека легких (НОЛ) и нейровоспаления. Согласно современным представлениям, существует несколько теорий развития НОЛ: вследствие нейро-сердечного или нейрогемодинамического отеков; «теория взрыва»; по причине адренергической гиперчувствительности легочной венулы; теория «двойного удара». Последняя основана на утверждении, что повреждение легких при ЧМТ возникает в ответ на системную воспалительную реакцию при появлении медиаторов этого процесса, продуцируемых глиальной тканью. Показано, что при ЧМТ развивается нейровоспалительный ответ, который способствует формированию острого респираторного дистресс-синдрома. Данные воспалительные явления сопровождаются продукцией и активацией комплементов, цитокинов, молекул адгезии и других многофункциональных пептидов. Причем нейровоспалительная активность при ЧМТ инициируется преимущественно в микроглии и астроцитах, что указывает на их ключевую роль в качестве мощного источника медиаторов воспаления. Также продемонстрировано, что развитие острого повреждения легких после ЧМТ связано с наличием экспрессии системного воспалительного ответа и НОЛ, пневмонии и т.д. В легочных тканях отмечается инициация функциональной активности клеток врожденного иммунитета на фоне массовой секвестрации интерстициальными нейтрофилами, которые затем мигрируют в альвеолы. В настоящее время необходимо проведение исследования роли различных молекулярных посредников, в том числе, эндотелина-1 в развитии патологии дыхательной системы, обусловленной ЧМТ.

The development of respiratory distress in traumatic brain injury (TBI) is associated with the occurrence of non-cardiogenic, neurogenic pulmonary edema (NPE) and neuroinflammation. According to modern concepts, there are several theories for the development of NPE: due to neuro-cardiac or neurohemodynamic edema; “blast theory”; due to adrenergic hypersensitivity of the pulmonary venule; theory of “double strike”. The latter is based on the assertion that pulmonary injury in TBI occurs in response to a systemic inflammatory reaction when mediators of this process produced by glial tissue appear. It has been shown that with TBI, a neuro-inflammatory response develops, which contributes to the formation of acute respiratory distress syndrome. TBI causes a neuro-inflammatory response, which contributes to the formation of acute respiratory distress syndrome. The inflammation after TBI is caused by the production and activation of complement, cytokines, adhesion molecules, and other multifunctional peptides. Along with this neuroinflammatory activity is initiated by microglia and astrocytes; therefore, cells of the central nervous system are a powerful source of inflammatory mediators in TBI. It has also been demonstrated that the development of acute lung injury after TBI is associated with the expression of a systemic inflammatory response and NPE, pneumonia, etc. In the lung tissue, the initiation of the functional activity of innate immunity cells is observed against the background of massive sequestration by interstitial neutrophils, which then migrate to the alveoli. At the moment, there is a need to study the role of various molecular mediators, including endothelin-1 in the development of respiratory system pathology due to TBI.

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