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Sodium oxybate
Last reviewed: 23.04.2024
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Sodium oxybate - sodium salt of GOMK; belongs to the class of hydroxycarboxylic fatty acids. It is close in structure to GABA, which participates in the natural metabolic processes of the mammalian brain, is one of the products of the Krebs cycle, participates in the synthesis of fatty acids, activates the pentose pathway of glucose-6-phosphate metabolism. The largest quantities are contained in the hypothalamus and basal ganglia. In addition, it is found in the kidneys, myocardium, skeletal muscles. GHB was discovered and synthesized long before the first clinical application in 1960 by the famous A. Labory. GHB can not overcome the BBB; this ability is given to it by the form of the sodium salt.
Sodium oxybate: a place in therapy
Benefits of sodium oxybate during the maintenance of anesthesia clearly manifested in anesthesia in elderly, weakened patients, against intoxication, liver and kidney failure. It is indicated to patients with severe endogenous intoxication, hypoxia of any etiology. It is also possible to combine with any inhalation and / or intravenous anesthetics. Due to the slow development of the hypnotic effect during induction, it was recommended to combine it with barbiturates. But a decrease in the total dose of sodium oxybate deprives it of its obvious merits. That is why sodium oxybate as a hypnotic is now used in a limited way (only in Russia, the former Soviet republics and selected countries in Europe).
In pediatrics, taking sodium oxybate or rectally is a good means of postoperative sedation. The ICU is used to adapt the patient to a respirator. Recently, this use of sodium oxybate has been criticized, which, however, should not relate to the severity of sedative-hypnotic properties of drugs, but to the methodology of conducting respiratory therapy.
In sodium obstetrics, oxybate is used for so-called therapeutic obstetric anesthesia. LS has a tranquilizing effect, relaxes the cervix, and at the same time increases the strength and frequency of uterine contractions and its sensitivity to oxytocin. Has an antihypoxic effect on the fetus. Sodium oxybate has found application in the treatment of alcoholism for arresting an arousal, a hangover and withdrawal symptoms.
Sodium oxybate does not provide a rapid onset of sleep. But, along with etomidatom, in recommended doses, it practically does not exert a depressing effect on hemodynamics.
Mechanism of action and pharmacological effects
The idea of the exact mechanism of action of sodium oxybate is contradictory. Despite the affinity with GABA, it does not directly act on its receptors. Sodium oxybate is not a precursor to GABA, as it was previously thought. It is assumed that the main mechanism for switching off consciousness is to block transmission at the postsynaptic level in the nuclei of the reticular formation and to directly inhibit the activity of the cortex. It inhibits GABA transaminase, promotes the accumulation of y-butyrolactate, as a result of which the activity of neurons is suppressed. At the level of the spinal cord inhibition of excitation and a decrease in muscle tone. In addition, sodium oxybate increases the concentration of dopamine in the brain. Adrenergic component of sodium oxybate is confirmed by a decrease in its activity at a high level of adrenaline in the blood against the background of the action of propranolol.
As a result of the dissociation between the thalamocortical and limbic systems, the anesthesia caused by ketamine is usually called dissociative.
Influence on the central nervous system
Sodium oxybate has a tranquilizing and hypnotic effect. The analgesic properties are weak. There is a pronounced dependence of the effect on the dose used, but sensitivity to drugs is individual. Sleeping occurs smoothly, without the stage of excitement. With rapid on / in the introduction of possible myoclonus and motor anxiety. In general, it has an anticonvulsant effect.
Electroencephalographic picture
EEG in the anesthesia of sodium oxybate is largely paradoxical and emphasizes the ambiguity of its influence on the interaction of the cerebral cortex and the reticular formation. Changes on EEG phase. The initial stages are characterized by epileptoid excitation. As the anesthesia deepens, the paroxysmal pattern is replaced by CNS depression with a slowing of the rhythm and a decrease in amplitude. There is a dissociation between the electrophysiological picture and the clinical state: a deep level of CNS depression in the EEG picture (sigma waves with periods of suppression) is clinically accompanied by superficial anesthesia.
Influence on the cardiovascular system
Sodium oxybate causes a certain decrease in heart rate, especially manifested in deep anesthesia. The effect on blood pressure is less pronounced. These shifts are leveled during surgical intervention because of insufficient CNS oppression.
In general, sodium oxybate has little effect on the cardiovascular system, and, according to many researchers, it is even stabilizing. In particular, the threshold of cardiac fibrillation increases. This determines the use of sodium oxybate in patients with a high risk of developing cardiovascular complications and with initial hemodynamic disorders, including hypovolemia and hemorrhagic shock.
Influence on the respiratory system
The effect of sodium oxybate on respiration is also not so great as that of other hypnotics. In therapeutic doses, the respiratory center is not depressed, breathing is reduced, but becomes deeper. This allows even short-term interventions with the patient's self-contained breathing saved. However, in relatively high doses, it causes a significant relaxation of the pharynx muscles and obstruction of the upper respiratory tract.
Effects on the gastrointestinal tract and kidneys
Sodium oxybate enhances mesenteric blood flow (almost twice), as well as stabilizes renal blood flow, increases glomerular filtration and diuresis. In addition, nartium oxybate optimizes the metabolism of the liver along the aerobic pathway. With a systematic admission, it lowers cholesterol, raises blood sugar levels. On protein metabolism and coagulability of the blood does not affect.
Effect on the endocrine response
Under the influence of sodium oxybate there is a temporary suppression of dopamine intake into brain cells, a significant increase in levels of growth hormone and prolactin. Along with this, protein synthesis (anabolic effect) is activated. The GCS level does not change significantly; there is some hyperinsulinemia. Typically, the increase in the level of ACTH (an advantage over this etimidate in patients with a reduced function of the adrenal cortex). It is assumed that the sodium-induced oxybite tendency to hypokalemia and hypernatremia is associated with its effect on the renin-angiotensin-aldosterone system.
Sodium oxybate significantly stimulates the function of the pituitary gland. Apparently, this determines his attribution to psychoenergetic drugs and sexual stimulants (aphrodisiacs).
[13], [14], [15], [16], [17], [18]
Effect on neuromuscular transmission
Sodium oxybate causes relaxation of skeletal muscles. The action is more central than peripheral.
Tolerance and dependence
When sodium oxybate is used, there is no physical dependence, but psychological addiction is possible.
Pharmacokinetics
The main way of sodium oxybate administration is IV. Allowed / m introduction. In children, the administration of the drug is administered orally or rectally.
Sleep occurs after 4-7 minutes from the beginning of the introduction into the vein. The maximum concentration in the blood is reached after 15 minutes. When administered orally, the effect begins 10-20 minutes, the peak concentration is reached after 20-60 minutes, the duration of action is 1-3 hours, the residual effects are possible within 2-4 hours. The clearance is 14 ml / kg / min. Sodium oxybate is metabolized almost completely to carbon dioxide and water (about 90% of the drug) and is eliminated by the lungs. Splitting occurs in the Krebs cycle in the tissues of the brain, heart, kidneys. Approximately 3-5% of unchanged medication is excreted by the kidneys.
Tolerance and side effects
Due to its "naturalness" for the body of sodium oxybate has a high therapeutic index. At recommended doses, it is usually well tolerated and does not have toxic effects. Side effects are most likely with the rapid administration and use of large doses of drugs. Excessive doses (more than 5 g) cause to whom. Toxic effects can be intensified when combined with other psychotropic drugs, including alcohol. Specific antidotes have not. The use of analeptics is ineffective, and therefore undesirable.
Pain when administered
With the introduction of sodium oxybate, the reaction from the side of the venous wall is practically absent.
Attempts to accelerate induction by increasing the rate of sodium oxybate administration can lead to the appearance of excitation, myoclonus and seizures. This can be avoided by the appointment of benzodiazepine premedication and the addition of small doses of barbiturates or ketamine.
Hemodynamic changes
Sodium oxybate only in high induction doses (more than 300 mg / kg) affects hemodynamics, which is manifested by a tendency to arterial hypotension and bradycardia.
Allergic reactions
Sodium oxybate is not histamine-liberator and usually does not cause allergic reactions.
Postoperative nausea and vomiting syndrome
Nausea and vomiting are more likely after taking sodium oxybate inside.
Reaction of awakening
In addition to the slow development of sleep, inertia and poor controllability, the shortcomings of anesthesia with sodium oxybate are also delayed awakening and the likelihood of excitation and vomiting. After awakening, patients experience a sensation of full sleep, a surge of energy and emotional comfort. In the postoperative period, drugs can cause dizziness.
Other effects
Sodium oxybate actively promotes the movement of potassium from the plasma into the cell. This is accompanied by hypokalemia and may require correction. But the addition of drugs to the polarizing mixture is extremely beneficial when it is necessary to increase the intracellular potassium concentration. This effect of sodium oxybate along with a decrease in the growth rate of azotemia has a positive effect in the treatment of renal failure.
Interaction
Sodium oxybate favorably combines with inhalation anesthetics, drugs for neuroleptanalgesia (NLA), ketamine, local anesthetics. GHB and narcotic analgesics, anesthetics, neuroleptics have a mutual potentiating effect. The combination with fentanyl enhances the depression of hemodynamics in comparison with its single use.
Attention!
To simplify the perception of information, this instruction for use of the drug "Sodium oxybate" translated and presented in a special form on the basis of the official instructions for medical use of the drug. Before use read the annotation that came directly to medicines.
Description provided for informational purposes and is not a guide to self-healing. The need for this drug, the purpose of the treatment regimen, methods and dose of the drug is determined solely by the attending physician. Self-medication is dangerous for your health.