This review summarizes studies on radial artery autograft vasospasms in coronary artery bypass grafting, and analyzes possible causes of grafted artery vasospasm. Coronary artery bypass grafting has proven the most effective method for correcting the consequences of coronary heart disease. Spasmophilia of arterial bypass grafts in the intraand postoperative period is currently amenable to pharmacological control. Arterial spasms are mediated by the tonic activity of smooth muscle cells in the vessel media in response to many different factors. The exact mechanisms of spasms and the reasons for their development remain unclear; however, clinical practice requires assessment of the functional bypass graft viability. The review analyzes possible causes of radial artery conduit vasospasms and existing methods for controlling the tone of arterial bypass grafts. Research in this area may expand the indications for the use of arterial bypass grafts and predict their long-term functional viability.

Recent studies in the integrated bases (PubMed, Science Direct and Scopus) have shown that urgent abdominal pathology in surgery leads to functional disorders of kidneys, acute kidney damage, and acute renal functional insufficiency. Without timely diagnosis and pathogenetically based treatment, many nephrological diseases lead to chronic renal functional insufficiency and terminal chronic renal insufficiency, a life-threatening condition that requires replacement therapy such as hemodialysis or kidney transplantation. The microcirculatory bed is the main link of the functional element of an organ – a spatially oriented structural and functional complex consisting of cellular and fibrous formations of a given organ or tissue. Numerous studies have proven that each organ has its own specific morphological structure, and therefore, specific features of the structure of functional elements. The structure of the microcirculatory bed is closely related to the structure of the organs and the formation of their structural and functional units, and the organization of the microcirculatory bed determines microhemodynamics and metabolism in organs and tissues. It is obvious that without a deep understanding of the morphofunctional changes that occur at the level of hemimicrocirculation in the kidneys during endotoxicosis and after its elimination, there can be no qualitative improvement in the pathogenetic therapy of patients with acute renal failure that complicates the course of various urgent surgical diseases. Clarifying the main stages of morphofunctional changes and morphometric indicators of the restructuring of intraorgan vessels in the kidneys and renal corpuscles in correlation with the temporal characteristics of the dynamics of the pathological process in the abdominal cavity will expand our understanding of the mechanisms of adaptation of the circulatory system, which is of theoretical and practical importance for medicine in general and, in particular, for emergency abdominal surgery.

This review presents literature data from the past 30 years on the microcirculation system in human skin in obesity. The data are analyzed separately using three types of noninvasive research methods – videocapillaroscopy, laser Doppler flowmetry, and photoplethysmography – which provide information on the structural and functional state of various components of the skin microvascular bed: the capillary (exchange link), precapillary (superficial vascular plexus), and deep vascular plexus (distribution link). At the capillary bed level, obesity is associated with changes in capillary shape and a decrease in their number. At the precapillary arteriolar level, impaired endothelial function and a reduced response to dilator stimuli are observed. Large distributing arterioles of the deep vascular plexus exhibit increased stiffness and resistivity indices. Most studies examine microcirculation in obese patients with associated conditions such as diabetes, metabolic syndrome, hypertension, and others, the presence of which can significantly impact microcirculatory blood flow parameters. Studies examining skin microcirculation in obese patients without any comorbidities are rare. A review of the literature also revealed no studies examining the structural and functional characteristics of microcirculation depending on the obesity phenotype.

Introduction. Adipose tissue produces a wide range of biologically active substances known as adipokines. Their imbalance in obesity leads to endothelial dysfunction. Given the «aging down» of metabolic syndrome, methods for early prediction and risk monitoring of vascular disorders are particularly relevant. In recent years, the triglyceride-glucose index (TyG), based on fasting triglyceride and glucose levels, has attracted the attention of researchers.

Aim. To study the characteristics of microcirculation in young overweight individuals at the different levels of the TyG index.

Materials and Methods. Fifty-six participants with overweight and stage I obesity, aged 17 to 26 years, were divided into 2 groups based on their TyG index. Group 1 included young adults with a TyG index ≤6.29 (n=28) and group 2 comprised those with a TyG index ≥6.3 (n=28). Anthropometric assessment included measurements of height, body weight, body mass index (BMI), waist and hip circumferences (WHI) and waist-to-hip ratio (WHR). Laboratory diagnostics involved measuring plasma glucose and triglyceride levels. To assess vascular wall function, photoplethysmography (PPG) and laser Doppler flowmetry (LDF) were performed.

Results. Analysis of gender distribution showed a predominance of males in the second group with higher TyG values. PPG analysis revealed no significant differences in microcirculation parameters between the two groups. LDF assessment revealed a decrease in the amplitude of endothelial vasomotions by 38.2% (p<0.05), myogenic vasomotions by 36.06% (p<0.05), and the amplitude of respiratory component indicators by 36.23% (p<0.05) in the group with increased TyG compared to group 1.

Conclusion. In young adults with overweight and stage I obesity, associated with a TyG index above 6.3 a.u., there is a decrease in the contribution of endothelial and myogenic components to the regulation of peripheral tissue microcirculation.

Introduction. The severity of lower extremity ischemia can be determined based on the ankle-brachial index (ABI), a noninvasive and widely available diagnostic method. Transcutaneous oximetry (tcpO₂) is one of the methods for assessing lower extremity blood flow not only at rest but also during exercise. This has prompted interest in studying the feasibility of assessing the severity of chronic lower extremity ischemia using this method.

Objective. To determine the correlation between transcutaneous oxygen tension (tcpO₂) values on the feet during exercise testing and the ABI value at rest in patients with occlusive-stenotic lesions of the lower extremity arteries.

Materials and Methods. This retrospective study included 34 patients (23 men and 11 women, mean age 69±4.9 years) with occlusive-stenotic lesions of the aortoiliac segment and lower extremity arteries. All patients were diagnosed with chronic ischemia stage IIb according to Fontaine-Pokrovsky. The patients underwent the following examinations: multislice computed tomography angiography and/or catheter angiography of the abdominal aorta and lower extremity arteries, tcpO₂ of the feet during exercise testing, and ABI calculation. Exclusion criteria were occlusivestenotic lesions of the lower extremity arteries preventing ankle pressure measurement, acute or chronic limb-threatening ischemia, and comorbidities limiting treadmill testing. We assessed the correlation between the ABI level and minimum foot tcpO₂ values at rest, measured sitting, standing, during and after treadmill walking, as well as their ratios at different measurement periods. The predictive ability of tcpO2 indicators in relation to the ABI level was also analyzed.

Results. No statistically significant correlation was found between absolute foot tcpO₂ values and ABI. The highest statistically significant (p=0.001) Spearman correlation coefficient (rho=0.48) was found between ABI and the ratio of foot tcpO₂ during the recovery period after exercise to the baseline value measured in a standing position before exercise. At a ratio below 0.84, the sensitivity and specificity for a decrease in ABI below 0.7 were 70% and 88%, respectively (p<0.001).

Conclusion. The ratio of foot tcpO₂ values during the recovery period after exercise to the same value measured in a standing position before exercise significantly correlates with the ABI value, and a value of this ratio below 0.84 may indicate subcompensated lower extremity ischemia.

Introduction. Remote ischemic preconditioning (RIPC) is a promising intervention for protecting organs and tissues from damage.

The aim of this study was to evaluate the diagnostic efficacy of angioneuroprotective biomarkers in patients with extrapyramidal movement disorders undergoing magnetic resonance-guided focused ultrasound (MRgFUS) thermocoagulation.

Materials and Methods. 42 patients were enrolled in a prospective, randomized, blinded study with an active control (sham RIPC). Prior to the procedure, patients were randomized into either the RIPC group (cuff pressure set at systolic blood pressure + 50 mm Hg, n=21) or the sham RIPC group (cuff pressure set at diastolic blood pressure, n=21). The protocol in both groups consisted of three 5-minute cycles of the cuff inflation (preconditioning or its imitation) each followed by a 5-minute rest intervals. Levels of biomarkers (TRIM72, S100B, ubiquitin, Lp-PLA2, endothelin-1) were measured in blood serum before and 1 hour after MRgFUS procedure.

Results. Comparison of post-procedural biomarker levels revealed statistically significant differences: the S100B levels were higher in the sham RIPC group (1.34 ng/mL) compared to the RIPC group (0.44 ng/mL, p<0.001) and the ubiquitin level (5.8 ng/mL) were also higher than in the RIPC group (4.73 ng/mL) (p = 0.008). These findings indicate that prior RIPC is associated with suppression of biomarkers of neuroglial damage (S100B) and proteolytic stress (ubiquitin) released in response to thermocoagulation.

Conclusion. RIPC is associated with reduced levels of S100B and ubiquitin during MRgFUS thermocoagulation, demonstrating a cytoprotective effect by mitigating blood-brain barrier and neuronal damage.

The aim of the study was to evaluate the degree of morphological changes in the wall of the great saphenous vein (GSV) associated with recurrent varicose veins at different intervals after endovascular laser ablation (EVLA) for varicose veins.

Material and methods. The study included thirty-two patients (20 women and 12 men) with symptomatic recurrent varicose veins treated at S. M. Kirov Military Medical Academy (Advanced Surgical Training Clinic № 1) between 2018 and 2020. They had previously undergone EVLA of the GSV trunk due to its insufficiency and varicose transformation, as well as miniphlebectomy. Twenty-four (75%) patients underwent open reoperation. Segments of the terminal sections of the GSV trunks with a length of 10–40 mm and sections of the GSV in the lower and middle third of the thigh were taken from 24 operated patients for morphological and microscopic analysis. A microscope at 40× to 200× magnification and hematoxylin and eosin staining were used. The histological examination results were evaluated using a semiquantitative analysis technique.

Results. In cases of early recurrence (1–3 months after surgery), focal isolated changes in all layers of the venous wall with signs of incomplete destruction of its tissue structures were detected in 3 patients (12.5%). At later stages (12 patients, 50%), pronounced irreversible changes in the media of the vessel were observed. In cases of varicose vein recurrence and vein recanalization after a period of more than 1 year (9 patients, 37.5%), collagen and elastic fibers at the site of the heat-induced thrombus contained a large amount of hyaline.

Conclusion. An assessment of the degree of structural changes in the vein wall previously treated with laser coagulation revealed that the key reason for the GSV recanalization within the first year after surgery is insufficient energy impact on all layers of the venous vessel.

Introduction. Cyclophosphamide-induced cardiotoxicity is one of the most severe complications of high-dose immunosuppressive therapy followed by autologous hematopoietic stem cell transplantation (HDIT-AHSCT). The early onset of myocardial dysfunction (within 2–10 days) limits the effectiveness of current monitoring strategies and necessitates the development of early prediction methods.

Objective. To develop predictive models for early identification of patients at high risk of myocardial dysfunction during autologous HDIT-AHSCT.

Materials and Methods. This observational cohort study included 74 patients with multiple sclerosis (mean age 36±8 years) undergoing autologous HDIT-AHSCT with high-dose cyclophosphamide. Assessments were performed before treatment and on days 3 and 7 of therapy. Cardiac biomarkers, electrocardiographic, and echocardiographic parameters were evaluated. Stepwise discriminant analysis was used to develop predictive models.

Results. Subclinical cardiotoxicity (NT-proBNP ≥534 pg/mL) was detected in 65 % of patients, while clinically manifest cardiotoxicity occurred in 5 %. A predictive model for subclinical myocardial dysfunction was developed, incorporating diastolic function parameters (E/A, ΔE/A, ΔE), left atrial volume, and hemoglobin level (sensitivity 96.8 %, accuracy 88.1 %). A model for predicting acute left ventricular heart failure was based on E/e’, serum urea levels, and changes in left ventricular mass (overall accuracy 97.3 %). Key alterations were detectable as early as day 3 of therapy.

Conclusion. The proposed models enable early identification of patients at high risk of cardiotoxicity during autologous HDIT-AHSCT. This provides an opportunity for timely treatment modification and prevention of severe cardiovascular complications.

Introduction. Bilateral ligation of the common carotid arteries in laboratory rats has become the gold standard for modeling cerebral hypoperfusion. Specialized literature demonstrates partial restoration of blood flow in the vascular territory of the common carotid arteries, which is due to the development of collateral blood flow pathways.

The aim of the study was to evaluate the intraorgan angioarchitectonics of certain neck organs under normal conditions and following bilateral ligation of the common carotid arteries in rats, in order to identify the characteristics of collateral blood flow pathway development during cerebral hypoperfusion.

Materials and methods. The study was conducted on 15 male Wistar rats. Four rats served as the intact control group, and 9 rats with a cerebral hypoperfusion model were euthanized at 8, 21, and 35 days post-operation; 2 rats died after the surgery. The vascular bed was injected with a black ink-gelatin mass.

Results. In the early stages (8 days), a decrease in blood filling of the hemocapillaries was observed in all studied neck organs. The most intensive growth of the collateral vessel network occurred in the fascial sheath of the cervical neurovascular bundle and its components—the internal jugular vein and the vagus nerve. By day 21 post-operation, the diameters of arterial anastomoses increased by 27.7 % in preparations of the proper fascia, by 40.1 % in the neck muscles, and by 18.5 % in the pharyngeal wall. Blood filling of the hemocapillaries increased. By day 35, major blood flow pathways were formed, which played the primary role in compensating for blood flow after bilateral common carotid artery ligation.

Conclusion. Thus, the development of collateral blood flow pathways during modeled cerebral hypoperfusion exhibits distinct stages.

Introduction. Lipids are major structural components of cell membranes and are involved in the regulation of neuronal membrane functions. Alterations in lipid metabolism are considered an important pathogenetic mechanism of acute cerebral ischemia.

Aim. To evaluate the effect of hypoxic preconditioning (HP) on the lipid composition of brain tissue and pulmonary pro-oxidant activity in rats with acute cerebral ischemia.

Materials and methods. Experiments were performed on 37 male outbred white rats weighing 180 – 230 g. Cerebral ischemia was induced by combined common carotid artery ligation. Neurological deficit was assessed using the Garcia scale. The lipid composition of brain tissue was analyzed by thin-layer chromatography, and lipid peroxidation intensity was assessed by measuring malondialdehyde concentration.

Results. In cerebral ischemia, animal survival was 20%, whereas HP increased survival to 34%. The Garcia score decreased from 18 in sham-operated animals to 10.9±0.5 after ischemia and was 13.1±0.4 in the HP group (p<0.05). In brain tissue, phosphatidylcholine, sphingomyelin, phosphatidylethanolamine and phosphatidylinositol concentrations decreased by 59.3%, 60.2%, 34.9%, and 37%, respectively, while lysophospholipids increased 3.79-fold. Ceramide levels increased 4.2-fold, whereas ceramide-1-phosphate decreased by 47.4%. HP reduced lysophospholipid and ceramide levels (1.9-fold) and increased ceramide-1-phosphate concentration 1.7-fold. In lung tissue, the malondialdehyde concentration increased 3.1-fold during ischemia and decreased 1.5-fold with HP.

Conclusion. Hypoxic preconditioning exerts systemic protective effects, partially normalizing brain lipid metabolism and reducing neurological deficit in cerebral ischemia.

Introduction. Experimental models of cerebral ischemia are widely used in preclinical studies, but they are often insufficiently adapted for studying thrombosis and thrombolysis in the microcirculation.

Objective. To develop a new approach for modeling focal infarction of the cerebral cortex in the parietal zone in rats.

Materials and Methods. The approach is based on the application of a cotton thread soaked in a 24.4% iron (III) chloride to the dura mater at the location of the pial arteriole.

Results. A 10-minute application was found to cause narrowing of the arteriole lumen and dilation of nearby venules, as well as a significant decrease in cerebral blood flow. After 24 hours, an infarction zone of approximately 22 mm² was formed in this area. Administration of tissue plasminogen activator (2 mg/kg, intra-arterially) at the beginning of the application suppressed occlusion, eliminated the decrease in cerebral blood flow (27.5 vs 3.3 PU, p<0.001), and significantly decreased the area of cerebral cortex damage (0.33 vs 22 mm², p<0.0001).

Conclusion. The developed method allows for intravital recording of microcirculation changes and it can be used to explore new approaches to thrombolytic therapy for stroke.

This article describes a patient with acute lower paraplegia, in whom spinal MR angiography failed to visualize the artery of Adamkiewicz, while the anterior spinal artery and the artery of Desproges-Gottteron were narrowed and shortened. MR tractography demonstrated unchanged fiber pathways in the lower spinal cord. This pattern of spinal vascular depletion proves the expediency of using spinal MR angiography for the differential diagnosis of myelopathies. In 1968, one of the pioneers of research on vascular spinal pathology, G. Lazorthes, wrote that «it becomes obvious to neurologists that spinal vascular pathology is not less common than cerebrovascular pathology. Neurological syndromes, previously referred to as myelitis, turn out to be vascular myelopathies in most cases» (Lazorthes, 1992). Modern neuroimaging techniques confirm this conclusion.