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The use of lithium salts in psychiatry has a long, more than two-thousand-year history. It goes back to the ideas of Hippocrates II, Galen and Soran of Ephesus regarding the feasibility of using mineral waters from certain sources, which, as we know today, were rich in lithium, magnesium and bromine salts, for the treatment of both manic and depressive states. Later, this effect of lithium salts was rediscovered – independently of each other – in the mid-19th century by the American psychiatrist William Alexander Hammond and the Danish psychiatrist Carl Lange. However, since this discovery was based on incorrect premises, namely, on the theory of «brain urine acid diathesis» as the cause of mental illness, it was not accepted, ignored and even ridiculed by colleagues. The rediscovery of the anti-manic effect of lithium salts by John Cade in 1948 is one of the greatest discoveries of psychiatry of the 20th century.The mechanisms of lithium therapeutic action are complex, diverse and not fully understood to this day. Initially, John Cade suggested that this effect of lithium is associated with its deficiency in patients with bipolar disorder and that exogenous lithium aids in compensation of such deficiency, or that patients with bipolar disorder suffer from some congenital disorder of lithium metabolism, thus requiring higher daily lithium doses than healthy people. However, it was soon shown that this was not the case.Despite the emergence of a significant number of alternative mood stabilizers, lithium remains relevant in psychiatry to this day.

Aim. Comparative measurement of concentration of lithium, circulating immune complexes and complement activity in animals’ blood and lymph in experimental anaphylactic shock and Arthus phenomenon. Methods. Experiments were conducted on 27 chinchilla rabbits in double series. The studied values of lithium, concentration of circulating immune complexes and complement activity in intact animals were used as controls. Results. On day 7 of sensibilisation before anaphylactic shock the titer of complement components in the blood decreased by 1.4 times (p

Organic lithium salts are a promising area for searching for effective and safe neuroprotective drugs. By using chronic bilateral common carotid artery occlusion models, the authors have previously found that lithium gluconate and lithium citrate are effective agents to prevent a neurological deficit in brain ischemic or neurodegenerative damages. The use of organic lithium salts in brain ischemia leads to their targeted accumulation in the frontal lobes of the brain and in the cerebrospinal fluid, normalizing trace elemental homeostasis in the brain Objective: to compare the neuroprotective effects of different lithium salts (chloride, carbonate, ascorbate, and citrate). Material and methods. A neurocytological study was performed using a glutamate-induced stress model in cultured granular neurons (CGNs). The state of CGNs was monitored daily and at each experimental stage, by viewing in an inverted phase contrast microscope. The final concentrations of the test substances in the culture medium were 0.1, 0.2, and 0.5, and 1 mM. The survival of CGNs was quantified by directly counting the neurons with intact morphology in 5 fields of vision. Five experiments were carried out for each substance. The number of neurons with intact morphology in the control cultures was taken as 100% survival. Results. Lithium chloride and lithium carbonate in the studied range of concentrations did not show significant neuroprotective properties. Lithium ascorbate and lithium citrate, on the contrary, significantly increased the survival of neurons in mild, moderate and severe glutamateinduced stress. Lithium citrate at a concentration of 0.2 mM increased the survival rate of CGNs by an average of 30% (p < 0.003). The active neuroprotective principles of lithium citrate were shown to be both lithium ion and citrate anion. These positive qualities of the test organic lithium salts are explained primarily by the fact that ascorbate and citrate anions contribute to the enhanced transport of lithium ions into the cells through appropriate ion channels for the transport of organic acids (SLC13A5, etc.). Conclusion. Lithium ascorbate and lithium citrate were confirmed to have an immediate neuroprotective effect on cerebellar CGNs. Treatment of CGNs with lithium citrate showed a 30% increase in cell survival during glutamate-induced stress.

Pharmaceuticals based on lithium ions have been already used in clinical practice for over 60 years for the treatment of bipolar disorders and remain a basic pharmacological therapy for patients with this disease. In spite of this, the therapeutic mechanisms of action of lithium ions have not been fully investigated. In the past decade, in vitro and in vivo experiments have provided a good deal of data suggesting that lithium ions have previously undescribed neuro-, cardio-, and nephro-protective properties. Numerous investigations have demonstrated that glycogen synthase kinase-3/3, the key enzyme of different pathological and protective signaling pathways, is the target of lithium ions in displaying these effects. This review deals with just these new properties of lithium ions, which make them utterly promising for clinical use in circulatory arrest-associated conditions, which is particularly relevant for anesthesiology and resuscitation. Key words: lithium ions, brain, heart, kidney, postresuscitation disease.