Objective: to study the impact of cerebral hypoxemia on the indicators of neuroinjury, by relying on the diagnosis of post- operative cognitive impairments, and the neuroinjury marker S100b protein and to examine the relationship of postoperative cognitive mpairments. Subjects and methods. Forty-eight non-cardiac surgical and non-neurosurgical patients with verified cerebrovascular disease, who had been operated on under total intravenous anesthesia with propofol and total myoplegia, were examined. Blood S100b protein levels were determined after cerebral hypoxemia detectable by transcranial oximetry. Postoperative delirium was diagnosed by the ICU-CAM test; postoperative cognitive dysfunction was diagnosed according to the Montreal cognitive assessment scale in the periods: 7 days, 1, 3, and 6 months, and 1 year, by using the control group, the Z scores of these indicators were standardized. Results. Cerebral desaturation led to early postoperative disorders, such as delirium and dysfunctions, in 72.7% of the cases. Cerebral saturation parameters correlated moderately, but significantly with neuropsychological indicators at 30 days of the study and 3 months after surgery and just stronger with S100b protein level. The risk of postoperative cognitive impairments in relation to the values of S100b protein was validly predicted in the models of logistic regression and ROC analysis. The rate of early and persistent cognitive dysfunction differed statistically significantly in patients with prior delirium; the logistic regression model validly predicted a relationship between this event and the neuropsychological indicators on 7 days postsurgery. Conclusion. In the patients with cerebrovascular diseases, cerebral hypoxemic episodes are dangerous. When they occur, there is an increased risk of postoperative cognitive impairments, including long-term problems. The above-threshold S100b protein concentration of 0.26 ng/mg is an early predictor of postoperative cognitive disorders. 

Objective: to investigate the influence of the A118G polymorphism of the μ-opioid receptor gene (OPRM1) on the course of total intravenous anesthesia. Subjects and methods. A sample consisted of 161 gynecological patients who had under- gone elective surgery under conventional total intravenous anesthesia. Heart rate, noninvasive mean blood pressure, peripheral oxygen saturation, bispectral index, and somatosensory evoked potentials were monitored in all the examinees before and after administration of the induction dose of an anesthetic, in the intraoperative and early postoperative period. The polymorphic variants of the gene in question were determined by allele-specific PCR. Results. According to the identified genotype, the patients were divided into 3 groups: 1) 118A/A genotype carriers (n=101); 2) 118A/G genotype carriers (n=48); 3) 118G/G genotype carriers (n=12). It was intraoperatively found that the 118G/G genotype carriers tended to have hypertension and to consume higher quantities of fentanyl and droperidol than the 118A/A and 118A/G carriers. The intergroup difference in the bispectral index was statistically insignificant during surgery. In the early postoperative period, the 118G-allele homozygotes showed a deeper level of sedation, which correlated with the significantly lower values of the bispectral index (p<0.01) and the higher incidence of adverse reactions (p<0.01). At the same time, the latency and amplitude of somatosensory evoked potentials in the 118G/G genotype carriers showed the least variations as compared to the A-allele homozygotes and heterozygotes (p<0.01). Conclusion. The A118G polymorphism of the μ-opioid receptor gene (OPRM1) affects the course of total intravenous anesthesia. The 118G/G genotype patients needed larger doses of narcotic analgesics, requiring a longer follow-up in the early postoperative period. 

The use of perfluorane for the cytoprotection of lung structures in gram-negative lung infections has been inadequately studied. Objective: to experimentally reveal the pattern of morphological changes in the lung during combined inhalation of lipopolysaccharide (LPS) and perfluorane that has cytoprotective properties. Materials and methods. The experiment was carried out on 35 outbred male albino rats weighing 320—350 g. The experimental animals were allocated to groups: 1) one-hour ventilation (controls) (n=5); 2) inhaled LPS 1.0 mg (n=10); 3) inhaled perfluorane 1.0 ml (n=10); 4) inhaled LPS 1.0 mg and then inhaled perfluorane 1.0 ml (n=10). Results. According to morphological findings, Group 1 (controls) was found to have no signs of lung structural changes. Group 2 (inhaled LPS) was noted to have signs of characteristic LPS-induced lung injury. Group 3 (inhaled perfluorane) showed complexes of macrophages with vacuolated cytoplasm (perfluorophages) in the bronchial lumen 3 hours after inhaled perfluorane administration. In Group 4, inhaled perfluorane exerted a cytoprotective effect: the degree of LPS- induced morphological changes in the lung was much lower than that in Group 2. Conclusion. The experimental model of LPS-induced lung injury indicated that LPS inhalation led to alveolar and bronchial epithelial damage, interstitial and alveolar edema, and obvious cell infiltration at the expense of lymphocytes, segmented leukocytes, and macrophages. This model showed that inhaled perfluorane reduced the signs of alveolar and bronchial epithelial damage and the degree of interstitial and alveolar edema. This supports clinical findings and offers possibilities of using inhaled perfluorane in resuscitation. 

Objective: to experimentally reveal possible systemic hemodynamic changes after maximally allowable liver resection, by determining the time of their formation in the early postoperative period. Materials and methods. The experiments on 22 outbred male albino rats recorded an electrocardiogram, left carotid blood pressure by a direct method, an integral rheogram and its first derivative by the tetrapolar rheographic procedure developed by Sh. I. Ismailov et al. and modified by V. V. Karpitsky et al. 1, 3, 6, and 12 hours and 1, 3, and 7 days after maximally allowable liver resection. Stroke volume, mean blood pressure, cardiac output, and specific peripheral vascular resistance (SPVR) were calculated. Blood loss was estimated by the gravimetric method. The significance of differences was defined by Friedman ANOVA. Results. At postoperative hour 1, the low cardiac output syndrome the basis for which is a considerable reduction in stroke volume developed and persisted during the first 24 hours; an additional contribution was made by moderate bradycardia observed within the first 24 hours. On day 3 postsurgery, the hemodynamic parameters were similar to those at baseline. By 7 day of an observation, cardiac depression changed into moderate myocardial hyperdynamia in the presence of moderate tachycardia and a moderate decrease in SPVR. Conclusion. The critical time found by the authors for the minimum cardiac output was an hour after surgery. The distinctive features of low cardiac output syndrome after maximally allowable liver resection are its reversible pattern and reflectory bradycardia on postoperative day 1. By day 7, cardiac depression changed into moderate myocardial hyperdynamia due to a tendency towards tachycardia. 

Objective: to study the structural bases of natural defense mechanisms of the human brain against chronic ischemia. Materials and methods. To accomplish this, histological, immunohistochemical (NSE, calbindin, NPY, p38) and morphometric examinations of intraoperative biopsy specimens were performed to determine the reorganization of excitatory and inhibitory neurons in the ischemic penumbra of the temporal cerebral cortex (CC). Morphometric analysis was made using the specially developed algorithms to verify neurons and their elements in the ImageJ 1.46 program. Results. The reduction in the total numerical density of neurons and synapses in chronic ischemia was ascertained to be accompanied by the compensatorily enhanced expression of NSE, calbindin, p38, and NPY in the remaining CC neurons. There were signs of hypertrophy of inhibitory CC interneurons and growth of their processes. In consequence, the impact of inhibitory CC interneurons on excitatory neurons was likely to enhance. Conclusion. In chronic ischemia, the human brain is anticipated to respond to damage to some cells via compensatory excitatory and inhibitory neuronal reorganization directed towards its natural defense against excitatory damage and towards better conditions for compensatory recovery of the structure and function of CC. 

Objective: to evaluate the effect of a 1.5% crystalloid polyionic Reamberin solution on cellular structures in children in the perioperative period. Subjects and methods. A randomized prospective study was conducted in 117 children aged 1 to 18 years during different surgical interventions under anesthesia with sevoflurane, fentanyl, or rocuronium to provide ASA I—II estimates. A study group included 55 children, in whom basic infusion therapy was switched to infusions of 1.5% Reamberin solution 20 minutes before the end of a surgical intervention. A comparison group comprised 62 children, in whom basic infusion therapy was switched to infusions of 0.9% NaCl solution 20 minutes before the end of surgery. In the study and control groups, the solutions were administered in a dose of 6—10 ml/kg depending on age at a rate of 2 ml/min. Results. 1.5% Reamberin solution was found to contribute to earlier and significant improvement in the function of cellular structures in children in the perioperative period. 

Objective: to master and practically execute cardiopulmonary resuscitation (CPR) procedural techniques, to acquire skills to use state-of-art equipment, and to teach work in the team. Subjects and methods. Forty-six interns and residents took a simulation course of training in basic CPR and automatic external defibrillation. Three-four days before the course, its participants received the certified translation of the European Resuscitation Council (ERC) information material and studied it. The course education program encompasses lectures, lessons on a medical care algorithm in sudden cardiac arrest, and practical works using models, including chest compression, ventilation, and automatic external defibrillator (AED) training. The duration of the course is 6—7 hours. Results. All the interns and residents were motivated to learn: to acquire first aid skills to manage sudden cardiac arrest. The ERC algorithm and a 4-stepped model to have practical skills were used. The taken course met expectations in 100% of the participants; all the interns and residents adequately acquired practical CPR skills and successfully completed their training. A questionnaire survey at the end of the course showed the high efficiency of the course. The training enhanced motivation in 29 interns and residents; they obtained an ERC provider degree; 10 interns and residents continue to take a course of training as an ERC instructor.