The aim of review is to discuss the results of studies on diagnosis of tissue hypoxia by laser-induced spectroscopy, as well as to identify promising trends and prospects of this technique for its further application in experimental and clinical medicine.

The review presents the findings of studies of the fluorescence intensity of endogenous fluorophore molecules (reduced nicotinamide adenine dinucleotide, oxidized flavin adenine dinucleotide) as markers of ischemic injury of internal organs (brain, heart, liver, kidneys, etc.). The principles of fluorescence laser-induced spectroscopy in vivo are discussed. The historical aspects of the subject are also covered. The results of the use of the technique in experimental and clinical studies of tissue hypoxia and ischemia are shown. Difficulties in interpreting the intensity values of autofluorescent signal of the studied molecules are revealed. It was noted that the tissue autofluorescence in a long-term anoxia remains unknown, and there are no structured ideas about the impact of exogenous and endogenous factors on autofluorescence intensity.

In conclusion, the use of laser-induced fluorescence spectroscopy to diagnose tissue ischemia is a promising area of experimental and clinical medicine, which still has various unresolved issues, despite a large number of studies in this domain.

This article discusses the importance of eliciting the mechanisms of action and the metabolism of microbiota in the critically ill patients, as well as the role of nutrition specialist in the management of these patients.

In critically ill patients the impaired regulation of endogenous metabolic processes and protein-energy deficiency are aggravated by abnormal microbiota metabolic processes. There is growing awareness of the importance of studying microbial metabolism in the general metabolic process. Its implications for the improved efficacy of treatment in critical care and rehabilitation are obvious.

Current international intensive care guidelines are being constantly revised in response to the new research data available on the mechanisms of critical illness. The course of the latter may significantly associate with the metabolic activity of human microbiota. Active management of metabolic processes is being sought through the subordination of bacterial metabolism to the interests of the host. Both antimicrobial and bioformulations (prebiotics, metabiotics) will be used in the long term in a targeted manner with the control of key microbial metabolites through available laboratory monitoring tools.

Based on the literature data and the original research, the author formulates postulates of the microbiota metabolism in critical illness, introduces the concepts of «invisible organ dysfunction» and «signaling bacterial molecules», offers answers to the eternal «what is to be done?» question and suggests using a number of microbial aromatic amino acids metabolites as an integral indicator of a course of critical illness.

The presence or development of liver disorders can significantly complicate the course of critical illness and terminal conditions. Systemic hemostatic disorders are common in Intensive Care Units patients with cholestatic liver diseases, so the study of the mechanisms of their development can contribute to the understanding of the development of multiorgan failure in critical illness.

The review discusses current data on changes in hemostatic parameters in patients with cholestatic liver diseases, proposes a mechanism for the development of such disorders, which involve interactions of phospholipids with platelet and endotheliocyte membranes. It is suggested that a trend for thrombosis in patients with cholestatic liver disease is due to increased accumulation of bile acids in the systemic circulation. Available data demonstrate that the antiphospholipid syndrome may predispose to the formation of blood clots due to alterations of phospholipid composition of membranes of platelets and vascular endothelial cells by circulating antiphospholipid antibodies. Clarifying the mechanisms contributing to changes of the blood coagulation system parameters in liver disorders will aid to development of optimal correction of hemostatic disorders in patients with chronic liver diseases.

The review focuses on the neuroprotective mechanisms of therapeutic hypothermia from the standpoint of metabolic depression and genomic reprogramming of neurons that develop when brain temperature decreases.

The concept of hypothermic pre-conditioning based on the development of typical nonspecific reactions for the formation of the cytoprotective phenotype of neurons due to potentially dangerous stimuli, such as ischemia, reperfusion, and hypothermia, was used to explain the effects of low temperatures. The data confirming the role of therapeutic cerebral hypothermia as a technique of selective brain exposure to mild cold for the neuroprotection and correction of temperature balance disorders are shown.

The approach to therapeutic hypothermia as a hypothermic pre-conditioning allows to significantly expand the scope of its use in various procedural variants.

The aim: To assess the effect of COMT G1947A genetic polymorphism (val158met) on the efficacy of spinal analgesia on day 1 after laparoscopic surgery for colorectal cancer.

Material and methods. In a pilot study involving 100 patients with colorectal cancer, operated through laparoscopic access, using spinal analgesia (10.0–12.5 mg of bupivacaine + 200 mcg of morphine), the frequency of COMT gene G1947A (val158met) polymorphism, the intensity of pain on day 1 after surgery, the frequency and severity of nausea, vomiting, skin itching, the need for additional analgesia have been assessed.

Results. The frequency distribution of alleles val/val (25%), val/met (45%) and met/met (30%) was consisted with Hardy-Weinberg equilibrium (χ2=0.96; P>0.05) and was not significantly different from the healthy donor group. In the groups of patients with various COMT alleles of val158met polymorphism, the studied parameters also did not differ significantly.

Conclusion. Study did not find significant link between spinal analgesia efficacy on day 1 after laparoscopic surgery for colorectal cancer and COMT rs4680 G1947A (val158met) polymorphism. Further research to enhance the power of the study is warranted to reach the final conclusions.

The aim of the paper: to identify promising diagnostic and prognostic biomarkers of pathological processes development based on the red blood cell membrane morphology and nanostructure in patients with brain disorders in the Intensive Care Unit.

Materials and methods. The study included 24 patients from the anesthesiology and resuscitation ward of the Federal Research and Clinical Center of Intensive Care Medicine and Rehabilitology. Blood was acquired from the patients for standard tests, and all further tests were performed in vitro. The images of red blood cells were obtained using the atomic force microscope «NTEGRA Рrima» (NT-MDT, Russia) in semi-contact mode.

Results. Patients from the anesthesiology and intensive care ward with traumatic brain injury, ischemic and hemorrhagic stroke, cerebral edema, and post-hypoxic encephalopathy had different blood cell shapes and localized defects of different topology on the surface of erythrocyte membranes including defects of pallor, torus, and nanostructure.

Conclusion. In this pilot study we have shown that several defects represent the trigger mechanisms for the development of a total membrane damage. Local topographic defects of nanostructures and abnormalities of erythrocyte morphology are irreversible. The number and quality of these abnormalities may eventually be used as a diagnostic and prognostic biomarker of pathological processes.

The Leiden Charter for Children in Hospital states that children in hospital shall have the right to have their parents or parent substitute with them at all times (European Association for Children in Hospital (EACH) 1988).

In this report, the technology chain for the implementation of the patient's parent/guardian resident stay model (RSM) in pediatric anesthesiology, resuscitation and intensive care unit (PARICU) was presented.

The aim of the report was to share the experience in improving patient safety and transparency of intensive care and introducing the active patient care through a «double control». The implementation of RSM has contributed to building a trustful interaction between parents/guardians and medical staff, developing skills for the proper care of children.

The 24-hour family-centered care in PARICU was favorably evaluated by parents/guardians and, according to preliminary data, helped to stabilize the condition and improve the well-being of patients.

Aim. To study the distribution and spatial organization of dentate gyrus (DG) astrocytes and CA4 area of hippocampus of Wistar rats following 20-minute occlusion of common carotid arteries (OCCA) compared to sham-operated control animals.

Material and methods. Histological (Nissl staining with hematoxylin and eosin), immunohistochemical (GFAP, MAP-2) and morphometric methods were used. Astrocytes and neurons in control (sham-operated animals, n = 5) group, after 6 hours (n=5), 1 days (n=5), 3 days (n=5), 7 days (n=5), 14 days (n=5) and 30 days (n=5) after 20-minute OCCA were studied on thin (4 µm) serial frontal sections of the hippocampus. Fractal analysis (ImageJ 1.52; fraclac 2.5 plugin) was used to obtain additional quantitative information on the spatial organization of astrocyte networks. Statistical hypotheses were tested using nonparametric criteria.

Results. 30 days after the 20-minute OCCA, only 5.3% of CA4 neurons were irreversibly destroyed and the total numerical density of DG granular cells remained at the control level. Hypertrophy and increased complexity of the spatial organization of astrocyte processes were observed 6 hours and 1 day after OCCA and persisted for 30 days. Astrogliosis was accompanied by an increased relative area of GFAP-positive material and fractal dimension and reduced lacunarity of the astrocyte network. The latter was especially evident in 1, 14 and 30 days after the OCCA.

Conclusion. After the 20-minute OCCA, the density of GFAP-positive material increased, the fibroarchitecture reorganized and gained more complexity due to the branching of astrocyte processes. At the same time, the total numerical density of neurons changed only slightly. All this indicated the probable role of astrocytes in post-ischemic activation of natural neuroprotection mechanisms.

Aim: to evaluate the impact of tissue-engineered structures (TES) transplantation based on mesenchymal stromal cell (MSC) sheets in myocardial infarction on the activation of the epicardial cell pool and vascularization of the damaged zone.

Materials and methods. Mesenchymal stromal cells were obtained from samples of subcutaneous fat of Wistar rats and C57Bl/6 mice. Tissue engineering structures were obtained by culturing cell sheets on thermosensitive plates (Nunc Dishes with UpCell Surface). Transplantation of TESs was performed after myocardial infarction modeling in rats by ligation of the anterior descending coronary artery. Transplant cells and damaged zones were assessed using immunofluorescent staining of myocardial cryosections. The impact of MSC secretion products on the migration activity of epicardial cells in vitro was evaluated using the explant culture method.

Results. MSCs in TESs after transplantation remain viable and induce activation of the epicardial cell pool and local increase of the damaged zone vascularization. The in vitro experiments showed that the conditioned environment of MSCs stimulates the migratory activity of epicardial cells and initiates the formation of activated Wt1/POD1 precursor cells.

Conclusion. TES transplantation on the basis of MSC sheets seems to be a promising approach for effective delivery of viable cells into myocardium to activate the epicardial cellular niche and reparative angiogenesis.