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It has been established that blood vessels are a target for influenza virus; however, the mechanism by which virus affects the cardiovascular system remains unknown. The aim of the study is the identification of histological changes and changes in the functional activity of the pulmonary and mesenteric blood vessels of Wistar rats. Wistar rats were intranasally infected with the influenza A(H1N1)pdm09 virus. At 24 and 96 h post infection (hpi), histopathological changes were observed in lung tissues with the absence of histological changes in mesenteric tissues. The functional activity of pulmonary and mesenteric arteries was determined using wire myography. In pulmonary arteries, there was a tendency towards an increase in integral response to the vasodilator and a decrease in the integral response to the vasoconstrictor at 24 hpi (compared with control). At 96 hpi, a tendency towards a decrease in the integral response to the vasoconstrictor persisted, while the response to acetylcholine was slightly increased. The functional activity of the mesenteric blood vessels was inverted: a significant decrease in the integral response to the vasodilator and an increase in the response to the vasoconstrictor at 24 hpi were observed; at 96 hpi, the integral response to the vasoconstrictor persisted, while the response to the vasodilator remained significantly reduced. Obtained data indicate the development of endothelial dysfunction in non-lethal and clinically non-severe experimental influenza virus infection.

The authors have analyzed research works, both by domestic and foreign researchers that dwell on frequency of H.pylori being resistant to antibacterial medications, the reasons for its occurrence, methods applied to determine it and ways to overcome it. Over the last 15 years there has been a growth in frequency of detecting H.pylori that was resistant to basic antibiotics used to eradicate the pathogen. The authors have established geographical diversity in resistance related to antibiotics intake by population. Bacteriological technique is the most valid for determining H.pylori sensitivity; however, it is rather difficult to apply it due to complicated procedures for the microorganism cultivation. Therefore, molecular-genetic techniques are widely used. H.pylori resistance to Clarithromycin has great practical significance as this antibiotic is able not only to produce antibacterial effects but also to destroy biofilms. Helicobacter that was resistant to Clarithromycin was the least frequently detected in northern European countries (1-3 %); it was the most frequently detected in Southern Europe, Asia,. Research performed in several Russian regions revealed significant variations in frequency of detecting H.pylori resistant to Clarithromycin (5-40 %) and a growth in dynamics of this detection (from 5 to 15 %). Frequency of detecting helicobacter resistance to another widely used medication, Metronidazole, is also different in different geographic regions; it amounts to 17 % in Europe, 24 % in Russia, and 92 % in Africa. H.pylori still has low resistance to Amoxicillin and another reserve medication, Rifabutin.The article also dwells on probable ways to overcome non-sensitivity of the pathogen to antibiotics and the necessity to develop procedures for treating H.pylori infection based on the results of examining the pathogen sensitivity with standardized techniques performed in different regions. Efficient H.pylori eradication reduces inflammation in the gastric mucosa, prevents ulcer formation and atrophy and reducers risks of stomach cancer.