Ultrastructural organization of pulmonary hemomicrovasculature in case of experimental acute renal failure

In our experiments on white male rats of Vistar line, we studied in dynamics (12, 24, 72 hours) the ultrastructural changes of pulmonary hemomicrovasculature in case of experimental acute renal failure. It has been determined that already in 12 hours after beginning of the experiment one can observe the ultrastructural constitution disorder of pulmonary hemomicrovasculature. In the capillary blood vessels of alveolar wall is determined the increased quantity of leukocytes, their adhesion and aggregation. With increase of the experimental period (24-72 hours), we have observed both dystrophic-destructive and compensatory-adaptive changes in pulmonary hemomicrovasculature

Correction of the ultrastructural changes of the respiratory department of the lungs by phosphatidylcholine liposomes due to multiple skeletal trauma with osteosynthesis in the experimental study

It was made the experimental study on white male rats by an electron microscopic method in dynamics (6, 24, 72, 168 h) and was studied the possibility of correction of ultrastructural changes of the respiratory department of the lung by phosphatidylcholine liposomes ("Lipin" medium) due to multiple skeletal trauma with the use of intramedullary osteosynthesis. It is defined that intraperitoneal Lipin administration in dose 50 mg/kg body weight during the first 24 hours after beginning of the study case decrease the expressiveness and prevalence of damage alveolar cells І and ІІ type, haemocapilari endothelial cells and alveolar macrophages. The Lipin administration does not influence on the character of ultrastructural changes of the respiratory department of the lung while increasing time of the experiment (72-168 hours)

Comparative characteristics of inducible NO synthase inhibitor and nitric oxide donor in endothelial dysfunction correction caused by osteoarthrosis under experimental conditions

Study have been carried out on white Wistar line rats (age – 3 months, weight – 180-220 g). According to the tasks the animals were divided into 7 groups. 1st group is intact (n = 20). 2nd group is rats, which were modeled osteoarthritis without further correction and were withdrawn from the experiment in the first stage (7th day) (n=40). 3rd group is rats, which were modeled osteoarthritis without further correction and removed from the experiment in the second stage (21st day) (n=40). 4th group is rats, in which experimental osteoarthritis was corrected with nonsteroidal anti-inflammatory drugs (NSAIDs) (Diclofenac) and aminoguanidine and removed from the experiment in the first stage (7th day) (n=20). 5th group is rats, in which experimental osteoarthritis was corrected with NSAIDs (Diclofenac) and aminoguanidine and withdrawn from the experiment in the second stage (21st day) (n=20). 6th group is rats, where experimental osteoarthritis was corrected using NSAIDs and a 7% L-arginine solution and withdrawn from the experiment in the first stage (7th day) (n=20). 7th group is rats, in which experimental osteoarthritis was corrected with NSAIDs and 7% L-arginine solution and withdrawn from the experiment in the second stage (21st day) (n=20) Animals were withdrawn from the experiment for the 7th day and the 21st day after the simulation of the pathological condition. NSAIDs (Diclofenac), aminoguanidine and L-arginine were administered from the beginning of the study. We have obtained the following results: The increase in the content of von Willebrand factor (VWF) in the animals blood proves that endothelial dysfunction is an important part of experimental osteoarthritis pathogenesis. It’s revealed the tendency which directed on normalization of the endothelial dysfunction investigated marker at correction by aminoguadine as a part of complex therapy. L-arginine involvement in the complex correction in experimental osteoarthritis more pronouncedly normalized the VWF level, which indicates the endothelial function normalization. The use of nitric oxide donor is more effective in comparison with the inhibition of inducible NO synthase also in the endothelial nitric oxide synthase activity analysis

Interdependence investigation of dynamic between the von Willebrand factor and erythrocyte and leukocyte intoxication indices in experimental peritonitis

The research was conducted on 175 white rats of reproductive age (3 months), weight of animals - 180-220 g. Animals were divided into 4 groups: Group 1 - 20 intact animals. Group 2 - 50 rats with simulated fecal peritonitis. Group 3 - 50 rats with simulated fecal peritonitis with subsequent antibiotic correction and debridement by chlorhexidine solution. Group 4 - 50 rats with simulated fecal peritonitis with subsequent antibiotic correction, chlorhexidine debridement and endothelial dysfunction correction with the use of a nitric oxide donor. Fecal peritonitis was modeled using injection of 10% fecal suspension in a dose of 0.5 ml per 100 g of animal weight in the abdominal cavity of laboratory animals by puncture method (Lazarenko V.A., et al., 2016, patent No. 233826). The following results were obtained. Endothelial dysfunction is the trigger mechanism of vascular catastrophes after experiencing experimental peritonitis. Evidence of endothelial functional status impairment during experimental peritonitis is a significant increase in the level of Willebrand factor in the animals blood flow (p <0.001). It was revealed significant increase in erythrocyte intoxication index (EII). It has been proved increase in leukocyte intoxication index (LII) in experimental animals during simulated peritonitis. It has been confirmed effectiveness of nitric oxide donor use in the complex correction of peritonitis and endothelial dysfunction as its complication is confirmed

The Condition of Pulmonary Hemomicrocirculatory Channel in Experimental Diabetes Mellitus

The aim of the study was to investigate the dynamics of ultrastructural changes in pulmonary hemocapillaries during experimental diabetes mellitus (DM). Experiments were performed on 40 white male rats Wistar. In the experimental group, diabetes was modeled by intraperitoneal streptozotocin administration, firm «Sigma» (USA), diluted in 0.1 M citrate buffer, pH 4.5, at the rate of 60 mg/kg. Development of the disease was monitored by the glucose levels growth in the animals’ blood. Collecting of lung tissue for electron microscopic examination was performed under general ketamine anesthesia after 1, 2 and 4 weeks after administration of streptozotocin. During the first 2 weeks of the study in the cytoplasm of pulmonary hemocapillaries endothelial was growing the number of micropinocytose vesicules, edema and expansion components of the Golgi complex and granular endoplasmic grid. There can be found erythrocytic sludges in some hemocapillaries. It was found that the most expressed changes in the hemomicrocirculatory channels appear 4 weeks after modeling diabetes. In the endotheliocyte of the pulmonary hemocapillaries there were observed vacuolation of the cytoplasm, swelling of cytoplasmic organelles, thickening of the basement membrane, adhesion and aggregation of blood cells. Thus, studies have shown that experimental diabetes is accompanied by ultrastructural changes of pulmonary hemomicrocirculatory channels components, the severity of which depends on the streptozotocin-induced DM progress

Ultrastructural Alterations in Alveolocytes of I Type Caused by Air Pollutants

Objective: to study in dynamics the ultrastructural alterations in alveolocytes of type I caused by air pollutants. Materials and methods: experiments were done on 72 white male rats of 180-220 grams of weight during 30, 60 and 90 days in 2 zones. Zone I – ecologically clean zone, zone II – distant part of the city with developed industry. The sampling of lung tissue for electronic-microscopic examination was carried out under ketamine anaesthesia following the common protocol. Results: there was established that in the conditions of industrial air pollution one can observe increase of quantity of micropinocytotic vesicles in the peripheral part of alveolocytes of I type already in 30 days after beginning of the experiment. As research period increases (60-90 days), in many alveolocytes of I type dystrophic destructive changes can be observed. Nuclei of such cells have round or oval form with clarified nucleoplasm. Perinuclear space is expanded. Mitochondria have matrix of weak electron-optical density and reduced cristas. The Golgi sacs and canaliculi as well as those of granular endoplasm grid are expanded. The quantity of ribosomes on membranes of the latter is decreased. In some cells we observed sailfin protrusions of plasma membrane towards air vesicle lumen. Also, we found the areas with local destruction of cell membrane of peripheral parts of alveolocytes of I type. Basal membranes are thickened with unclear contours. At the same time, we found alveolocytes of I type with characteristics of increased functional activity. Conclusions: continuous stay of experimental animals in the conditions of industrial air pollution is accompanied by expressed changes of ultrastructural organization of alveolocytes of I type. Degree of expressiveness and character of changes in alveolocytes of I type depends on duration of time from the moment of primary alteration of air pollutants.

СТІЙКІСТЬ ДЕЯКИХ БЕТОНІВ В РОЗЧИНАХ БОРФТОРИСТОВОДОРОДНОЇ КИСЛОТИ

The paper concerns the issue of boron-fluoro-hydrogenous acid (BFH) water solutions influence on concretes, usually used as flooring materials. A considerable destructive effect of this acid is demonstrated, which can be explained by combined influence of high acidity and the action of the hydrogen fluoride. There has been established an inhibiting effect of the super-plasticizer «Mapefluid» upon the destruction speed and hypotheses have been presented as for the mechanism of such effect.Исследовано действие водных растворов борфтористоводородной (БФВ) кислоты на бетоны, обычно используемые в качестве напольных материалов. Показано значительное разрушающее действие кислоты, обусловленное комбинированным влиянием высокой кислотности и фторида водорода. Установлено наличие ингибирующего влияния суперпластификатора «Mapefluid» на скорость разрушения и высказаны гипотезы по поводу механизма этого влияния.Досліджено дію водяних розчинів борфтористоводородної (БФВ) кислоти на бетони, які використовуються для матеріалів підлоги. Показано значну дію кислоти, яка руйнує, обумовлену комбінованим впливом високої кислотности і фториду водня. Установлена наявність інгібіруючого впливу суперпластифікатора «Mapefluid» на швидкість руйнування і висловлені гіпотези з приводу механізму цього впливу

Дослідження рівнів амінокислот в скловидному тілі експериментальних тварин при регматогенному відшаруванні сітківки

The article presents the results of studying the levels of amino acids in the vitreous body of rats with rhegmatogenous retinal detachment at different stages of modeling the pathology (on the 3rd, 5th and 7th day). In animals with modeling RRD, was observed a significant increase in the level of alanine, aspartate, glycine, glutamic acid compared with rats of conditionally intact group; maximum changes in indicators were observed on the 7th day of the study. The obtained data are explained by significant neurochemical changes of the glutamatergic system of the neural retina, which cause excitotoxicity (as a result of massive release of neuronal glutamate) and structural changes. In the study of the level of valine, histidine, tyrosine, phenylalanine and methionine, it was found that these amino acids are not involved in the pathogenesis of RRD, so their level does not change. The obtained experimental data deepen the existing pathophysiological data on the pathogenetic links of rhegmatogenous retinal detachment in the early stages of its progression, which is important for practical ophthalmology to develop effective pharmacotherapy of this disease.В статі представлені результати вивчення рівнів амінокислот в скловидному тілі щурів при регматогенному відшаруванні сітківки на різних термінах моделювання патолгії (на 3-у, 5-у та 7-у добу). Встановлено, що у тварин, яким моделювали РВС, спостерігали достовірне підвищення рівня аланіну, аспартату, гліцину, глутамінової кислоти порівняно із щурами умовно інтактної групи; максимальні зміни показників відмічено на 7-у добу дослідження. Одержані дані пояснюються значними нейрохімічними змінами глутаматергічної системи нейрональної сітківки, що викликають ексайтотоксичність (як результат масивного викиду нейронального глутамату) та структурні зміни. При дослідженні рівня валіну, гістидину, тирозину, фенілаланіну та метіоніну встановлено, що дані амінокислоти не беруть участь в патогенезі РВС, тому їх рівень не змінюється. Отже, можна припустити, що тривалість експериментального відтворення РВС має безпосередньо прямий негативний вплив на рівень амінокислот – тривала дія підвищеного рівня глутамату, аланіну та гліцину призводить до більш суттєвого пошкодження сітківки та незворотних змін в ній із розвитком некрозу. Одержані експериментальні дані поглиблюють існуючі патофізіологічні дані щодо патогенетичних ланок регматогенного відшарування сітківки на ранніх етапах їх прогресування, що має важливе значення для практичної офтальмології з метою розробки ефективної фармакотерапії даного захворювання