In recent years, the treatment of acute pain syndrome has been considered as an independent direction in anesthesiology and intensive care. New schemes of postoperative analgesia and new drugs developed by pharmacologists are actively being introduced. One of the newer regimens for pain relief is patient-controlled analgesia (CPA) or on-demand analgesia. The development of the concept of fast track surgery, one of the most widely discussed areas for the development of innovative technologies in modern surgery, from the point of view of the anesthesiologist of the resuscitation specialist, minimizes the stress response of the body to surgical aggression at all stages of the perioperative period. Increasingly, the method of preemptive analgesia is used more widely, based on the use of analgesics before the start of the operation, which helps to prevent the occurrence of peripheral and central sensitization.
The study of neural plasticity and related memory functions is one of the fundamental fields in anesthesiology. Understanding this issue is very important both for the physician - the anesthesiologist-resuscitator, and for the patient. This review of the literature describes structures and processes of the central nervous system which in a sense are the target for the amnestic action of sedation and anesthesia medications. The possibilities of implicit and explicit memory formation depending on different levels of sedation and anesthesia are considered. Special attention is paid to the mechanism of action of GABAergic drugs on the processes of memory consolidation and reconsolidation.
The objective was to evaluate the effect of propofol and dexmedetomidine sedation on the short-term memory and long-term memory consolidation.Materials and methods. 80 patients with small orthopaedic interventions under subarachnoid anesthesia were included in the randomized controlled trial. Three groups were formed depending on the drug used: group P – propofol, group D – dexmedetomidine, group 0 – control. Emotionally neutral sets of words were tapped three times to evaluate the effect of sedation on long-term memory consolidation: stage1/set 1 – immediately before sedation (RASS 0, BIS 95–100), stage 2/set 2 – 5–10 minutes after the start of sedation (RASS «–1» – «–2», BIS 70–90), stage 3/set 3 – 10 minutes after sedation was terminated and consciousness was recovered (RASS 0, BIS 90–100). In addition, the impact of sedation on the ability to hold the received information in short-term memory was conducted 5 minutes after the presentation of the words at stage 2. Reproduction and recognition testing of all words was conducted the next day after operation to evaluate the effect of medical sedation on long-term memory consolidation.Results. Propofol and dexmedetomidine provided an inhibitory effect on the ability to hold information in short-term memory compared to control group (р < 0.001 и р < 0.001, respectively). Propofol had the most effect on short-term memory and the level of its amnesic effect was associated with the cognitive function of patients (p = 0.013, R² = 0.23, β = 0.472). The HADS points were as negative predictor of the reproduction of the word set 1 in control group (p = 0.05, R² = 0.136, β = –0.368) and recognition of the word set 3 in propofol group (р = 0.029, R² = 0.176, β = –0.420). Within 24 hours after operation, reproduction and recognition of word sets 2 depended on the degree of short-term memory impairment during sedation (F(1.65) = 19.317, p < 0.001, ηp2 = 0.229 и F(1.65) = 21.638, p < 0.0031, ηp2 = 0.250, respectively). Short-term memory test acted as a positive predictor of the reproduction of word set 3 in control group (p = 0.05, R² = 0.141, β = 0.376).Conclusion. Propofol and dexmedetomidine impair the ability to retain information in short-term and, consequently, long-term memory, and propofol has a more pronounced amnesic effect, which depends on the cognitive functions of patients. The sensitivity to the amnesic effect of the drugs depends on the individual characteristics of the patients.
The aim of the study was to determine the changes in the levels of various neurotransmitters depending on the depth of propofol-induced sedation.Material and methods. Twenty-four patients were included in a prospective, simple blinded study. All patients underwent elective orthopedic intervention with subarachnoid anesthesia and moderate (group 1, n=12) or deep (group 2, n=12) propofol-induced sedation. Peripheral blood sampling for measurement of neurotransmitter levels was performed before regional blockade (Stage 1), 35–40 min after the start of sedation (Stage 2), and 10–15 min after sedation was terminated and consciousness was recovered (Stage 3).Results. Deep propofol-induced sedation resulted in a decrease in norepinephrine level at stages 2 and 3. Under moderate sedation, its level decreased at Stage 2 and returned to baseline after restoration of consciousness. The initial concentration of norepinephrine (Stage 1) was higher in Group 2.Conclusion. Propofol-induced sedation resulted in reduced level of the main stress hormone, which suggests its stabilizing effect on autonomic nervous system.
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