No abstract

In vivo studies of the therapeutic effects of argon in traumatic brain injury (TBI) are limited, and their results are contradictory. The aim of this study was to evaluate the effect of a three-hour inhalation of argon (70%Ar/30%O2) after an open TBI on the severity of the neurological deficit and the degree of brain damage in rats. The experiments were performed on male Wistar rats (n = 35). The TBI was simulated by the dosed open brain contusion injury. The animals were divided into three groups: sham-operated (SO, n = 7); TBI + 70%N2/30%O2 (TBI, n = 14); TBI + 70%Ar/30%O2 (TBI + iAr, n = 14). The Neurological status was assessed over a 14-day period (using the limb-placing and cylinder tests). Magnetic resonance imaging (MRI) scans and a histological examination of the brain with an assessment of the volume of the lesions were performed 14 days after the injury. At each of the time points (days 1, 7, and 14), the limb-placing test score was lower in the TBI and TBI + iAr groups than in the SO group, while there were no significant differences between the TBI and TBI + iAr groups. Additionally, no differences were found between these groups in the cylinder test scores (day 13). The volume of brain damage (tissue loss) according to both the MRI and histological findings did not differ between the TBI and TBI + iAr groups. A three-hour inhalation of argon (70%Ar/30%O2) after a TBI had no neuroprotective effect.

The impairments of cerebral blood flow microcirculation brought on by cardiac and respiratory arrest were assessed with multi‐modal diagnostic facilities, utilising laser speckle contrast imaging, fluorescence spectroscopy and diffuse reflectance spectroscopy. The results of laser speckle contrast imaging show a notable reduction of cerebral blood flow in small and medium size vessels during a few minutes of respiratory arrest, while the same effect was observed in large sinuses and their branches during the circulatory cessation. Concurrently, the redox ratio assessed with fluorescence spectroscopy indicates progressing hypoxia, NADH accumulation and increase of FAD consumption. The results of diffuse reflectance spectra measurements display a more rapid grow of the perfusion of deoxygenated blood in case of circulatory impairment. In addition, consequent histopathological analysis performed by using new tissue staining procedure developed in‐house. It shows notably higher reduction of size of the neurons due to their wrinkling within brain tissues influenced by circulation impair. Whereas, the brain tissues altered with the respiratory arrest demonstrate focal perivascular oedema and mild hypoxic changes of neuronal morphology. Thus, the study suggests that consequences of a cessation of cerebral blood flow become more dramatic and dangerous compare to respiratory arrest.

The overactivation of inflammatory pathways and/or a deficiency of neuroplasticity may result in the delayed recovery of neural function in traumatic brain injury (TBI). A promising approach to protecting the brain tissue in TBI is xenon (Xe) treatment. However, xenon’s mechanisms of action remain poorly clarified. In this study, the early-onset expression of 91 target genes was investigated in the damaged and in the contralateral brain areas (sensorimotor cortex region) 6 and 24 h after injury in a TBI rat model. The expression of genes involved in inflammation, oxidation, antioxidation, neurogenesis and neuroplasticity, apoptosis, DNA repair, autophagy, and mitophagy was assessed. The animals inhaled a gas mixture containing xenon and oxygen (ϕXe = 70%; ϕO2 25–30% 60 min) 15–30 min after TBI. The data showed that, in the contralateral area, xenon treatment induced the expression of stress genes (Irf1, Hmox1, S100A8, and S100A9). In the damaged area, a trend towards lower expression of the inflammatory gene Irf1 was observed. Thus, our results suggest that xenon exerts a mild stressor effect in healthy brain tissue and has a tendency to decrease the inflammation following damage, which might contribute to reducing the damage and activating the early compensatory processes in the brain post-TBI.

РЕЗЮМЕНастоящий обзор посвящен применению катетеризации сосудов мелких лабораторных животных в практике биомедицинских исследований с акцентом на технологические аспекты метода. Использование сосудистых катетеров для отбора проб крови, введения препаратов или с целью биомониторинга позволяет повысить качество исследования (достоверность и воспроизводимость результатов) и способствует соблюдению биоэтических норм. С современных позиций рассмотрены ключевые факторы, от которых зависит успех операции и всего исследования. В частности, даны рекомендации по выбору сосуда, типа и размера катетера в зависимости от особенностей животного и задач исследования. Подробно описана операция катетеризации наружной яремной вены крысы, принципиальные этапы которой одинаковы для всех магистральных сосудов грызунов. Также большое внимание уделено потенциальным осложнениям катетеризации сосудов, особенностям ухода за катетеризированным животным в послеоперационном периоде и мероприятиям, направленным на поддержание проходимости катетера и его надлежащего функционирования. Основными ограничениями широкого применения метода катетеризации в научных исследованиях являются недостаточная квалификация хирурга и необходимость использования операционного оборудования и микрохирургических инструментов.Ключевые слова: катетеризация яремной вены, сосудистый катетер, хроническая катетеризация, экспериментальная хирургия, мелкие лабораторные животные.Конфликт интересов. Авторы декларируют отсутствие явных и потенциальных конфликтов интересов, связанных с публикацией настоящей статьи.Источник финансирования. Авторы заявляют об отсутствии финансирования при проведении исследования.