Lithium Chloride Effect on Mortality and Neurological Deficits in the Model of Ischemic Stroke in Rats
The relevance of the problem of ischemic stroke is difficult to overvalue in modern terms. The data on the frequency of occurrence and outcomes, especially among young people, force us to look for new strategies to minimize its consequences. Recent experimental studies have shown pronounced neuro-cardio-nephroprotective properties of lithium salts. AIM OF STUDY To evaluate the effect of lithium chloride on the lethality and severity of cognitive and neurological deficits in the modeling of ischemic stroke in rats. MATERIAL AND METHODS The study used mongrel male rats weighing 312±12.5 g. The model of Longa's focal ischemia was used as a basis. The animals were divided into 5 groups: false-operated, control (model of ischemic stroke with the introduction of 0.9% NaCl) and three groups with the introduction of lithium chloride in various concentrations (4.2 mg/kg, 21 mg/kg and 63 mg/kg). The drug was administered daily for 14 days with a parallel assessment of neurological deficits. RESULTS According to the results of the experiment, the following data were obtained with respect to lethality in the studied groups: false - operated 0 out of 8, control group - 13 out of 22 (lethality 59%), group 3 (LiCl 4.2 mg/kg) - 8 out of 14 (lethality 57%), p>0.05 with respect to control, group 4 (LiCl 21 mg/kg) - 6 out of 15 (lethality 40%) p>0.05 with respect to control and in group 5 (LiCl 63 mg/kg) - 4 out of 15 animals died (lethality 27%) p=0.0317. Lithium chloride at doses of 21 mg/kg and 63 mg/kg resulted in a decrease in the severity of neurological deficits on the second day of the experiment. On the 15th day of the experiment, there were no differences in the severity of neurological disorders. Also, the dosage of 63 mg/kg contributed to better memory retention during the assessment of cognitive functions. CONCLUSION Lithium chloride at a dosage of 63 mg/kg significantly (p=0.037) reduced the mortality and severity of neurological deficits in the simulation of experimental ischemic stroke in rats compared to the control group.