A review of the literature is devoted to the analysis of the role of the autonomic nervous system as the main regulator of the body's homeostasis in heterotopic (anoxia, craniocerebral trauma, cerebral circulation disorder) brain damage. First of all, clinical, pathophysiological definitions and methods of pharmacological correction of manifestations of sympathetic and parasympathetic hyperactivity (paroxysmal sympathetic hyperactivity - PSH, paroxysmal parasympathetic hyperactivity - PPH) are considered first. An important aspect of the review is the evaluation of publications devoted to the prevention and therapy of systemic inflammatory response and secondary neuroinflammation based on functional adaptive responses of the autonomic nervous system. The mechanisms of the so- called cholinergic anti-inflammatory pathway to systemic and local inflammatory reactions are discussed. The aspects of the influence of the norm and pathology of the autonomic nervous system on the metabolism and energy balance of the organism are described in detail. The prospects of normalizing the nutritional status through therapeutic effects on the structures of the autonomic nervous system located in the hypothalamic zones of the brain, changes in the regulatory influences of parasympathetic and sympathetic nerves, the innervating liver, intestine, and pancreas are estimated. The interactions of peripheral structures of the autonomic nervous system and microbiota are considered separately. The relationship is shown in detail and possible mechanisms of the functional status of the sympathetic or parasympathetic nervous system in muscular dystonia, respiratory insufficiency and veining are discussed from the point of view of evaluation and correction of the most important constant of autonomic instability in the form of peripheral chemoreceptor insufficiency.
Dysfunction of the autonomic nervous system (ANS) of the brain in sepsis can cause severe systemic inflammation and even death. Numerous data confirmed the role of ANS dysfunction in the occurrence, course, and outcome of systemic sepsis. The parasympathetic part of the ANS modifies the inflammation through cholinergic receptors of internal organs, macrophages, and lymphocytes (the cholinergic antiinflammatory pathway). The sympathetic part of ANS controls the activity of macrophages and lymphocytes by influencing β2-adrenergic receptors, causing the activation of intracellular genes encoding the synthesis of cytokines (anti-inflammatory beta2-adrenergic receptor interleukin-10 pathway, β2AR-IL-10). The interaction of ANS with infectious agents and the immune system ensures the maintenance of homeostasis or the appearance of a critical generalized infection. During inflammation, the ANS participates in the inflammatory response by releasing sympathetic or parasympathetic neurotransmitters and neuropeptides. It is extremely important to determine the functional state of the ANS in critical conditions, since both cholinergic and sympathomimetic agents can act as either anti-or pro-inflammatory stimuli.
Background.At the same time, the main effect of the use of this drug is the elimination of the autonomic nervous system dysfunction and sympatholysis. It seems important to search for a method of indications and selection of a dose of dexmedetomidine in intensive care.Aims to improve the clinical effectiveness of the electrophysiological navigation of the prolonged use of dexmedetomidine in patients with brain pathology of various origins.Methods.The study included 83 patients 2050 days after the traumatic brain injury, anoxic damage; consequences of acute disorders of cerebral. 37 patients comprised the 1st intervention group with a clinical course of dexmedetomidine (male 28; female 9; average age 49.62.3 years) and 46 patients comprised the 2nd control group without pharmacological correction with dexmedetomidine (male 23; female 23, average age 512.5 years). Criteria for the inclusion of prolonged infusion of the drug dexmedetomidine (Orion Pharma, Finland) are based on heart rate variability (HRV) indicators characteristic of sympathetic hyperactivity, the target task of titration of doses of dexmedetomidine served as the parameters for achieving normal HRV indicators, the appearance of parasympathetic hyperactivity served as the basis for reducing the dosage of the drug or stopping it of application. HRV parameters were recorded before dexmetomedine infusion-initially, on 13; 45; 910; 1520 days of drug administration.Results.The starting dose of dexmedetomidine with sympathetic hyperactivity in patients was 0.12 to 0.24 g.kg1.hr1(average dose 0.160.01; total 200 mg/day). According to digital data from HRV, the effective dose of dexmedetomidine ED50 was 0.260.03 g.kg1.hr1(total daily 353.835.1 g) and was achieved on day 910 using dexmedetomidine.Conclusions.The protective role of dexmedetomidine with correction of sympathetic hyperactivity based on electrophysiological navigation according to the HRV is reliable in the following indicators: The improvement of consciousness; a significant decrease in the incidence of distress lung syndrome; septic shock; mortality.
The outcome in a chronic critical illness (CCI) after cerebral catastrophes occurs in 5-10% of patients in intensive care units and is accompanied by severe homeostasis disorders with a likely outcome in multiple organ failure. In this aspect there is a need for a deep study of the pathogenesis of a CCI with the identification of the most significant outcome criteria Purpose of the study: To reveal the prognostic in formativeness of functional activity and serum albumin concentration in patients in a CCI with different disease outcomes. Materials and methods: A comparative retrospective study was carried out of the concentration and functional activity (detoxifine efficiency - DTE) of serum albumin in 19 deceased (Group1) and 38 survived patients (Group 2) after cerebral catastrophic injury resulting in CCI. Samples for the study were obtained at the admission of patients, in the middle of the treatment and before discharge of patients. Results: It was established that in Group 1 the average value of albumin concentration and DTE decreased significantly, while in Group 2 values increased from the moment of admission to the discharge of patients. A ROC-analysis demonstrated a sufficiently high diagnostic informativeness of albumin DTE and concentration criteria, that differed in patients of Group 1 and 2 throughout all phases of the study. Conclusions: The outcome to a CCI after cerebral catastrophes is accompanied by changes in the concentration of serum albumin and violations of its functional activity – DTE. In patients with a fatal outcome, in contrast to patients with a positive effect of treatment, there is a progressive decrease in the concentration of serum albumin, which is combined with a pronounced decrease in its functional activity
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