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Sodium oxybate
Last reviewed: 04.07.2025
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Sodium oxybate is the sodium salt of GHB; it belongs to the class of oxycarboxylic fatty acids. It is close in structure to GABA, which participates in natural metabolic processes of the mammalian brain, is one of the products of the Krebs cycle, participates in the process of fatty acid synthesis, and activates the pentose pathway of glucose-6-phosphate metabolism. It is found in the largest quantities in the hypothalamus and basal ganglia. In addition, it is found in the kidneys, myocardium, and skeletal muscles. GHB was discovered and synthesized long before its first clinical use in 1960 by the famous A. Laborit. GHB cannot overcome the blood-brain barrier; this ability is imparted to it by the form of the sodium salt.
Sodium oxybate: place in therapy
The advantages of sodium oxybate during anesthesia maintenance are clearly evident during anesthesia in elderly, weakened patients, against the background of intoxication, liver and kidney failure. It is indicated for patients with severe endogenous intoxication, hypoxia of any etiology. It can also be combined 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 the reduction in the total dose of sodium oxybate deprives it of its obvious advantages. That is why sodium oxybate as a hypnotic is now used in a limited way (only in Russia, the former Soviet republics and certain European countries).
In pediatrics, sodium oxybate taken orally or rectally is a good means of postoperative sedation. In the intensive care unit, it is used to adapt the patient to a respirator. Recently, this use of sodium oxybate has been criticized, which, however, should not be related to the severity of the sedative-hypnotic properties of the drug, but to the methodology of respiratory therapy.
In obstetrics, sodium oxybate is used for so-called therapeutic obstetric anesthesia. The drug 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. It has an antihypoxic effect on the fetus. Sodium oxybate has found application in the treatment of alcoholism to relieve agitation, hangovers and withdrawal symptoms.
Sodium oxybate does not provide rapid onset of sleep. However, along with etomidate, in recommended doses it has virtually no depressing effect on hemodynamics.
Mechanism of action and pharmacological effects
The exact mechanism of action of sodium oxybate is controversial. Despite its affinity with GABA, it does not act directly on its receptors. Sodium oxybate is not a precursor of GABA, as was previously believed. It is assumed that the main mechanism of switching off consciousness consists in blocking transmission at the postsynaptic level in the nuclei of the reticular formation and direct inhibition of cortex activity. It inhibits GABA transaminase, promotes the accumulation of y-butyrolactate, resulting in the suppression of neuronal activity. At the level of the spinal cord, excitation conduction is inhibited and muscle tone decreases. In addition, sodium oxybate increases the concentration of dopamine in the brain. The adrenergic component of the action 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.
Due to the occurrence of dissociation between the thalamocortical and limbic systems, anesthesia caused by ketamine is usually called dissociative.
Effect on the central nervous system
Sodium oxybate has a tranquilizing and hypnotic effect. Analgesic properties are weak. There is a pronounced dependence of the effect on the dose used, but sensitivity to the drug is individual. Falling asleep occurs smoothly, without the stage of excitement. With rapid intravenous administration, myoclonus and motor restlessness are possible. In general, it has an anticonvulsant effect.
Electroencephalographic picture
EEG during sodium oxybate anesthesia is largely paradoxical and emphasizes the ambiguity of its effect on the interaction of the cerebral cortex and reticular formation. Changes in EEG are phasic. The initial stages are characterized by epileptoid excitation. As anesthesia deepens, the paroxysmal picture is replaced by CNS depression with a slowing of the rhythm and a decrease in amplitude. Dissociation is observed between the electrophysiological picture and the clinical state: a deep level of CNS depression according to the EEG picture (sigma waves with periods of suppression) is clinically accompanied by superficial anesthesia.
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Effect on the cardiovascular system
Sodium oxybate causes some slowing of the heart rate, especially evident during deep anesthesia. The effect on blood pressure is less pronounced. These changes are leveled out during surgery due to insufficient CNS depression.
In general, sodium oxybate has a minor effect on the cardiovascular system, and, according to many researchers, it even has a stabilizing effect. 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.
Effect on the respiratory system
The effect of sodium oxybate on respiration is also not as great as that of other hypnotics. In therapeutic doses, the respiratory center is not depressed, breathing slows down, but becomes deeper. This allows even short-term interventions to be carried out while the patient's independent breathing is preserved. However, in relatively high doses, it causes significant relaxation of the pharyngeal muscles and obstruction of the upper respiratory tract.
Effects on the gastrointestinal tract and kidneys
Sodium oxybate increases mesenteric blood flow (almost twice), and also stabilizes renal blood flow, increases glomerular filtration and diuresis. In addition, sodium oxybate optimizes liver metabolism by the aerobic pathway. When taken systematically, it reduces cholesterol levels and increases blood sugar levels. It does not affect protein metabolism or blood clotting.
Effect on endocrine response
Sodium oxybate causes temporary suppression of dopamine entry into brain cells, significant increase in somatotropic hormone and prolactin levels. Along with this, protein synthesis is activated (anabolic effect). The level of GCS does not change significantly; some hyperinsulinemia occurs. Typically, the level of ACTH increases (advantage over etomidate in patients with reduced adrenal cortex function). It is assumed that the tendency of sodium oxybate to hypokalemia and hypernatremia is associated with its effect on the renin-angiotensin-aldosterone system.
Sodium oxybate significantly stimulates the pituitary gland function. Apparently, this determines its classification as a psychoenergetic agent and sexual stimulant (aphrodisiac).
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Effect on neuromuscular transmission
Sodium oxybate causes relaxation of skeletal muscles. The action is central rather than peripheral.
Tolerance and dependence
When using sodium oxybate, physical dependence does not occur, but psychological addiction is possible.
Pharmacokinetics
The main route of administration of sodium oxybate is intravenously. Intramuscular administration is also permitted. In children, the drug is administered orally or rectally.
Sleep occurs 4-7 minutes after the start of intravenous administration. The maximum concentration in the blood is achieved after 15 minutes. When taken orally, the effect begins after 10-20 minutes, the peak concentration is achieved after 20-60 minutes, the duration of action is 1-3 hours, residual effects are possible for 2-4 hours. Clearance is 14 ml / kg / min. Sodium oxybate is metabolized almost completely to carbon dioxide and water (about 90% of the drug) and eliminated by the lungs. Splitting occurs in the Krebs cycle in the tissues of the brain, heart, kidneys. About 3-5% of the unchanged drug is excreted by the kidneys.
Tolerability and side effects
Due to its “naturalness” for the body, sodium oxybate has a high therapeutic index. In recommended doses, it is usually well tolerated and does not have toxic effects. Side effects are most likely with rapid administration and use of large doses of the drug. Excessive doses (more than 5 g) cause coma. Toxic effects may increase when combined with other psychotropic drugs, including alcohol. It has no specific antidotes. The use of analeptics is ineffective and therefore undesirable.
Pain when inserted
When sodium oxybate is administered, there is virtually no reaction from the venous wall.
Attempts to accelerate induction by increasing the rate of sodium oxybate administration may result in agitation, myoclonus, and seizures. This can be avoided by prescribing a benzodiazepine and adding small doses of barbiturates or ketamine.
Hemodynamic shifts
Sodium oxybate only in high induction doses (more than 300 mg/kg) affects hemodynamics, which is manifested by a tendency towards arterial hypotension and bradycardia.
Allergic reactions
Sodium oxybate is not a histamine liberator and does not usually cause allergic reactions.
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Postoperative Nausea and Vomiting Syndrome
Nausea and vomiting are more likely after taking sodium oxybate orally.
Awakening reactions
In addition to the slow development of sleep, inertia and poor control, the disadvantages of anesthesia with sodium oxybate are also slow awakening and the likelihood of agitation and vomiting. After awakening, patients experience a feeling of full sleep, a surge of strength and emotional comfort. In the postoperative period, the drug can cause dizziness.
Other effects
Sodium oxybate actively promotes the movement of potassium from plasma into the cell. This is accompanied by hypokalemia and may require correction. But adding the drug to the polarizing mixture is extremely beneficial when it is necessary to increase the intracellular concentration of potassium. The above action of sodium oxybate, along with a decrease in the rate of increase in azotemia, has a positive effect in the treatment of renal failure.
Interaction
Sodium oxybate is favorably combined with inhalation anesthetics, drugs for neuroleptanalgesia (NLA), ketamine, local anesthetics. GHB and narcotic analgesics, anesthetics, neuroleptics have a mutual potentiating effect. Combination with fentanyl increases hemodynamic depression compared to 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.