Reanimatology (the science of resuscitation) represents the science of critical illness, terminal and postresuscitation conditions, originated within the walls of the V. A. Negovsky Research Institute of General Rean-imatology, Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology, turns 85 years old on October 19, 2021. This editorial briefly describes the history of the development of the Institute, as well as the current scientific achievements of the Institute staff.

Aim of the study: to determine the predictive value of central hemodynamic parameters in relation to mortality and evaluate their potential acceptability for goal-directed therapy during days 1-4 of treatment in patients with sepsis.
Material and methods. The results of investigation and treatment of 62 patients aged 50.9±2.13 years with abdominal sepsis were analyzed. The patient severity on admission to the intensive care unit was 13 [10-15] on the APACHE II scale, 8 [6.75-9.25] on the SOFA scale. Lethal outcome 15.6±1.4 days after admission occurred in 19 (31%) patients. Central hemodynamic parameters were studied by transpulmonary thermodilution according to the standard technique. Infusions and administration of sympathomimetic drugs were performed according to Sepsis-3 guidelines. Statistical analysis was performed using logistic regression and ROC analysis.
Results. The median values of the main circulatory parameters during days 1-4 of sepsis treatment were within normal ranges. Cardiac index, afterload-related cardiac performance, global cardiac ejection fraction and cardiac function index were predictors of mortality at all stages of treatment. However, the first three parameters did not provide either sufficient model quality at the study stages or a stable cutoff value with acceptable sensitivity and specificity. The cardiac function index maintained good model quality (area under the ROC curve 0.708-0.753) and a stable cutoff value (≤5.75 to ≤5.81 min-1) with acceptable and balanced sensitivity and specificity of about 70% at all study stages.
Conclusion. The cardiac index, afterload cardiac performance, global cardiac ejection fraction and cardiac function index during days 1-4 of intensive care of sepsis are predictors of lethal outcome. At the same time, only the cardiac function index maintains good model quality and consistent cut-off point value with acceptable sensitivity and specificity at all stages of the study. The feasibility of using the cardiac function index as one of the parameters of goal-directed therapy aimed at cardiovascular function improvement in sepsis needs further investigation.

According to epidemiological studies, the leading cause of morbidity, disability and mortality are cerebrovascular diseases, in particular ischemic and hemorrhagic strokes. In recent years considerable attention has been given to the study of molecular markers of ischemic and hemorrhagic strokes. These studies are relevant because brain-specific protein biomarkers of neurons and glial cells can provide valuable and timely diagnostic information necessary for clinical decision-making.
The aim of the study was to reveal the differences in the serum level of molecular markers in acute, subacute and early recovery periods of ischemic and hemorrhagic strokes.
Material and methods. The study included 59 patients. Twenty patients were diagnosed with hemorrhagic stroke and 39 had ischemic stroke. The control group included 20 volunteers. Serum levels of molecular CNS markers were determined in acute, subacute, and early recovery stages of stroke. The serum levels of CNS molecular markers of patients with ischemic and hemorrhagic stroke was measured quantitatively by enzyme immunoassay. Statistical analysis was performed by nonparametric Mann-Whitney method.
Results. The level of brain-derived neurotrophic factor (BDNF) in the control volunteers was 574.5 [455.5; 615] pg/ml. Significant differences were found for acute and subacute periods of hemorrhagic stroke: it was 674 [560; 749] pg/ml (P=0.003) and 664 [616; 762] pg/ml (P=0.0001).
The level of neuron-specific enolase was significantly increased in all periods of the study: it was 4.15 [3.53; 4.8] ng/ml in the control group, 5.4 [4.4; 6.4] ng/ml in acute period of ischemic stroke (P<0.001), 5.4 [4.4; 6.4] ng/ml in early recovery period of ischemic stroke (P=0.001), 5.1 [4.6; 6.4] ng/ml in acute period of hemorrhagic stroke (P=0.014), 664 [616; 762] ng/ml in subacute period of hemorrhagic stroke (P=0.003).
In the control group, the serum S-100 protein level was 4.5 [3.8; 5.4] ng/ml. In the acute and early recovery periods of ischemic stroke, S-100 protein level has significantly fallen down to 4.1 [3.4; 4.6] ng/ml (P<0.031) and 3.9 [3.4; 6] ng/ml (P=0.014), respectively. Glial-cell derived neurotrophic factor level was 1.98 [1.64; 2.1] ng/ml in the controls and increased up to 2.4 [2.2; 5] ng/ml (P=0.002) in the acute period and 2.4 [2.3; 2.6] ng/ml (P<0.001) in the subacute period of hemorrhagic stroke.
The vascular endothelial growth factor receptor-1 (VEGFR-1) was significantly lower in the subacute period of hemorrhagic stroke: 485 [211; 945] pg/ml in the subacute period vs 903.5 [626; 1115] pg/ml in the controls (P=0.001).
Conclusion. We found differences in the serum level of molecular markers in patients with ischemic and hemorrhagic strokes. In the acute period, early recovery period of ischemic stroke, and subacute period of hemorrhagic stroke, there was an increase in the serum level of neuron-specific enolase. The level of brain-derived neurotrophic factor increased significantly in the acute and subacute periods of hemorrhagic stroke. In the acute and early recovery periods of ischemic stroke, the level of S-100 protein decreased. The level of glial cell-derived neurotrophic factor increased in the acute and subacute periods of hemorrhagic stroke. In the subacute period of hemorrhagic stroke, the level of endothelial growth factor receptor-1 significantly decreased. Moreover, there was significant difference between values of this parameter in the subacute period of hemorrhagic stroke and in the early recovery period of ischemic stroke.

Blood pressure dysregulation and circulatory failure are major contributors to the progression of sepsis and especially septic shock. One of the genes affecting the vascular endothelium and arteriolar tone is the angiotensin II receptor 1 gene (AGTR1). The AGTR1 rs275651 single-nucleotide polymorphism is associated with the development of angina, high altitude pulmonary edema, and hypertension. The significance of the AGTR1 rs275651 polymorphism in sepsis, particularly in patients with significant comorbidity, has not been studied previously.
The aim of the study was to determine the impact of AGTR1 functional polymorphism on sepsis outcome in patients with various comorbidities, including cardiovascular disease and type 2 diabetes mellitus.
Material and methods. A prospective study included 144 ICU patients of two clinical hospitals in Moscow, aged 18-75 years with clinical signs of sepsis (Sepsis-3, 2016).
Results. In the group of patients with cardiovascular diseases, carriers of the TT AGTR1 rs275651 genotype had a lower mortality rate compared with carriers of the A allele (25 deaths out of 33 versus 16 out of 16, respectively, P=0.041, Fisher's exact test; P=0.0019, log-rank test). In the group of patients with diabetes mellitus (n=62), we also found significant differences in sepsis outcome based on the AGTR1 rs275651 genotype variant. The subgroup of TT AGTR1 rs275651 genotype carriers demonstrated significantly lower mortality compared with TA, AA genotypes carriers (27 deaths out of 41 and 20 out of 21, respectively, P=0.012, Fisher's exact test; OR=10.37; 95% CI: 1.26 to 85.5; P<0.0001, log-rank test).
Conclusion. We found an association of the functional polymorphism AGTR1 -777 T>A (rs275651) with sepsis outcome in ICU patients with high-value baseline comorbidity: carriers of the more common TT genotype had lower mortality compared to carriers of the minor A allele.

The Aim: analysis of the influence of dispatcher assistance during cardiopulmonary resuscitation (CPR) of patients with out-of-hospital cardiac arrest (OHCA) in achieving return of spontaneous circulation (ROSC), better survival at the scene, survival to discharge, and 30-day survival.
Materials and methods. This study includes epidemiological data on OHCA collected by the study protocol of the European Resuscitation Council's EuReCa_ONE study during the period October 1, 2014 — December 31, 2019. Statistical analysis was performed using SPSS Statistics v26 and GraphPad Prism v8 software packages.
Results. This study included 288 patients with OHCA where CPR was provided by bystander. Dispatcher-assisted CPR (DA-CPR) occurred in 56.9% of those patients and ROSC was achieved in 31.3% of cases. Forty-four patients were hospitalized and 16 of those survived until discharge. There was no influence of dispatcher assistance on ROSC, although it resulted in slightly greater risk of the absence of ROSC (OR=1.063). Higher mortality rate to discharge occurred in DA-CPR group (P=0.013). No statistical significance was observed between DA-CPR and non-DA-CPR groups in terms of death at the scene, and 30-day survival. Dispatcher assistance during the initial CPR in hospitalized OHCA patients was a significant predictor of death outcome during hospitalization (P=0.017, OR=5.500).
Conclusions. There is no significant association between the presence/absence of dispatcher assistance and ROSC or 30-day survival rate. In contrast, DA-CPR was non-significantly associated with slightly higher odds for the absence of ROSC. DA-CPR was also associated with lower survival-to-discharge rates in hospitalized OHCA patients. The study findings are the base/ground which highlights the need of implementation of existing and development of new guidelines regarding high-quality professional training of EMS dispatchers as well as basic life support education of general population.

The human electroencephalogram (EEG) constitutes a nonstationary, nonlinear electrophysiological signal resulting from synchronous firing of neurons in thalamocortical structures of the brain. Due to the complexity of the brain's physiological structures and its rhythmic oscillations, analysis of EEG often utilises spectral analysis methods.
Aim: to improve clinical monitoring of neurophysiological signals and to further explain basic principles of functional mechanisms in the brain during anaesthesia.
Material and methods. In this paper we used Empirical Mode decomposition (EMD), a novel spectral analysis method especially suited for nonstationary and nonlinear signals. EMD and the related Hilbert-Huang Transform (HHT) decompose signal into constituent Intrinsic Mode Functions (IMFs). In this study we applied EMD to analyse burst-suppression (BS) in the human EEG during induction of general anaesthesia (GA) with propofol. BS is a state characterised by cyclic changes between significant depression of brain activity and hyper-active bursts with variable duration, amplitude, and waveform shape. BS arises after induction into deep general anaesthesia after an intravenous bolus of general anaesthetics. Here we studied the behaviour of BS using the burst-suppression ratio (BSR).
Results. Comparing correlations between EEG and IMF BSRs, we determined BSR was driven mainly by alpha activity. BSRs for different spectral components (IMFs 1-4) showed differing rates of return to baseline after the end of BS in EEG, indicating BS might differentially impair neural generators of low-frequency EEG oscillations and thalamocortical functional connectivity.
Conclusion. Studying BS using EMD represents a novel form of analysis with the potential to elucidate neurophysiological mechanisms of this state and its impact on post-operative patient prognosis.

The aim is to study the current aspects of resident training in anesthesiology and intensive care. The article focuses on the theoretical training of residents, the importance of a thorough knowledge of pathophysiology, and the formation of clinical thinking. Opportunities for the use of innovative educational computer technologies in residency training are shown. A consistent interdisciplinary pedagogical interaction makes it possible to improve the outcomes of residency training by achieving the main goal of developing a physician who has acquired universal, general and specific professional competences and is capable of providing high-quality medical care.

Results from recent large randomized trials investigating the use of high PEEP in patients without ARDS all suggest that high levels may increase mortality due to hypotension and bradycardia. A careful assessment of cardiac function — with particular focus on the right ventricle — should be performed before planning our ventilation strategy in any setting, including COVID-19 and ARDS in general. Mechanical ventilation should be respectful in regards of heart function, and tolerant with moderate hypoxia and hypercapnia, noninvasive (whenever possible) and synchronized.

Currently, a number of experimental studies have demonstrated compelling evidence of neuro-, cardio-, and nephroprotective properties of medications containing lithium chloride.
Aim of the study. To evaluate the effect of various concentrations of lithium chloride on ischemic stroke volume and perifocal edema in rats after cerebral ischemia.
Material and methods. Male mongrel rats weighing 315±13.5 g were used in the study. The focal ischemia model according to Longa et al. was employed. The animals (n=35) were divided into 5 groups: sham-operated, control group (ischemic stroke model with NaCl 0.9% administration) and three groups who received lithium chloride in different concentrations (4.2 mg/kg, 21 mg/kg and 63 mg/kg). Lithium chloride was administered immediately after cessation of middle cerebral artery occlusion and then every 24 h until euthanasia. To assess the degree of brain damage, the animals underwent magnetic resonance imaging (MRI) on day 2, and brain sections stained with 2,3,5-triphenyltetrazolium chloride were evaluated after euthanasia on day 7. Intergroup differences were assessed using the Mann-Whitney criterion.
Results. According to MRI data, lithium chloride at a dose of 4.2 mg/kg had no significant effect on ischemic stroke volume and perifocal edema versus the control group on day 2 (P=0.9). With lithium chloride at 21 mg/kg, stroke volume and perifocal edema were significantly lower than in the control group (by 25%, P=0.04 and 18%, P=0.03, respectively). Lithium chloride at a dose of 63 mg/kg was more likely to reduce stroke volume (by 45%, P=0.004) and perifocal edema (by 35%, P=0.007). When determining lesion volume on day 7, the data were comparable to those obtained on day 2. With the 21 mg/kg dose, stroke volume was 20% lower than in the control group (P=0.04). Lithium chloride, 63 mg/kg, reduced stroke volume by 40% (P=0.004).
Conclusion. Lithium chloride dose affects necrotic focus formation and manifestations of perifocal cerebral edema after middle cerebral artery occlusion. The maximum reduction in the volume of ischemic stroke and perifocal edema was observed when the 63 mg/kg dose was used.

The aim of the study. To examine the changes in structure and morphometry in sensorimotor cortical edema with cell swelling in mature white rats after common carotid artery occlusion of various durations.
Material and methods. Acute ischemia was modeled on white adult Wistar rats by 20-, 30- and 40-min occlusion of the common carotid arteries (CCA). Histological (hematoxylin-eosin and Nissl staining), immunohistochemical (NSE, MAP-2, GFAP) and morphometric methods were used. Morphometry was assessed on hematoxylin and eosin-stained specimens using ImageJ 1.53 plug-ins (Find Maxima, Find Foci). Statistical hypothesis testing (nonparametric criteria) was performed using Statistica 8.0 software.
Results. In the sensorimotor cortex (SMC) of white rats after 20, 30 and 40 minutes of CCA occlusion the signs of cytotoxic brain edema appeared, focal destructive and adaptive changes of neurons and astroglia evolved. The edema persisted throughout the observation period (7 days). The increase in the relative area, the number of cell swelling zones and their hydration (pixel brightness) was significant. On days 1 and 3 after CCA occlusion, some of the SMC astrocyte processes underwent destruction. Subpial and perivascular zones suffered to a greater extent. Mild and moderate (after unilateral 30-min CCA occlusion) to moderate and severe (after bilateral 40-min CCA occlusion) scattered structural and functional changes of the SMC with large areas of clearing in the «porous» neuropil, severe perivascular and perineuronal edema of the astrocyte processes developed. The latter was associated with a moderate reduction of the total neuronal density.
Conclusion. After occlusion of CCA, signs of edema with cellular swelling appeared in the SMC amid dystrophic and necrotic pyramidal neurons and activated neuroglial cells. To a greater extent, the signs of brain swelling were evident three days after bilateral 40-min occlusion of CCA.