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Journal articles on the topic 'Mildronate'

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Published: 10 March 2023

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1

Pupure, Jolanta, Juris Rumaks, Sergejs Isajevs, Olga Korzakova, Jelena Puncule, Simons Svirskis, Ivars Kalviņš, and Vija Kluša. "Mildronate's protective effects in the peripheral nervous system: stavudine-induced neuropathy and formalin-induced inflammation." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 64, no. 3-4 (January 1, 2010): 114–18. http://dx.doi.org/10.2478/v10046-010-0032-7.

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Mildronate's protective effects in the peripheral nervous system: stavudine-induced neuropathy and formalin-induced inflammation Mildronate, previously known as a cardioprotective drug, recently was found to normalise mitochondrial processes by preventing the dysfunction of complex I in rat liver mitochondria. Previously we have shown also the ability of mildronate to prevent pathologies in the central nervous system by normalizing the expression of different signalling molecules in brain tissue. This allowed us to suggest that mildronate may possess a beneficial role also in peripheral nervous system pathologies. The present study was designed to assess the peripheral tissue damage caused by anti-HIV drug stavudine, as well as pain and inflammation caused by formalin. For this demonstration, we investigated the influence of mildronate: (1) on decreased myelin expression and increased neuron degeneration in rat sciatic nerve tissue caused by stavudine; and (2) on formalin-induced inflammation in mice. We found that mildronate protected the stavudine-induced degeneration of neurons in rat peripheral sciatic nerve without a significant influence on demyelination. In a formalin test, mildronate showed anti-inflammatory action comparable to that of indomethacin, a reference drug. The present results show that mildronate is capable of regulating peripheral nerve damage and peripheral inflammatory responses. We suggest that the multifunctional effects of mildronate can be attributed to its ability to regulate mitochondrial processes. The obtained data indicate protective effects of mildronate in different peripheral neurological pathologies.

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Pupure, Jolanta, Sergejs Isajevs, Ivars Kalviņš, and Vija Kluša. "Protective effects of mildronate in indinavir- and efavirenz-induced toxicity in mice." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 64, no. 3-4 (January 1, 2010): 119–24. http://dx.doi.org/10.2478/v10046-010-0025-6.

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Protective effects of mildronate in indinavir- and efavirenz-induced toxicity in mice Previously we showed that mildronate effectively protected mice heart tissue against the toxic influence of anti-HIV drugs azidothymidine, stavudine and lamivudine, which belong to nucleosideanalogue reverse transcriptase inhibitor (NRTI) class. Recently we also demonstrated that mildronate protected isolated rat liver mitochondria against mitochondrial damage caused by azidothymidine. The present study was devoted to examine the possible protective effectiveness of mildronate in cardio-, hepato- and neurotoxicity models caused by anti-HIV drugs of other classes: indinavir, a representative of protease inhibitor (PI) class, and efavirenz, a non-nucleoside-analogue reverse transcriptase inhibitor (NNRTI). Drugs were administered intraperitoneally for two weeks, at the dose of 50 mg/kg of anti-HIV drugs and 100 mg/kg for mildronate. Afterwards, mice heart, liver and brain tissue were examined morphologically and immunohistochemically. The results showed that indinavir in heart tissue caused inflammatory and degenerative changes, manifested as increased expression of nuclear factor kappaBp65 (NF-kBp65), as well as cardiomyocyte necrosis and cellular infiltration. Efavirenz did not cause pathological changes in mice heart tissue, whereas it induced marked expression of caspase-3 and glial fibrillary acidic protein (GFAP) in mice brain tissue and small degenerative alterations in mice liver tissue. The data obtained show mildronate's protective properties in indinavir-induced cardiotoxicity and efavirenz-induced neurotoxicity.

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3

Prous, J., and J. Castañer. "MILDRONATE." Drugs of the Future 14, no. 1 (1989): 29. http://dx.doi.org/10.1358/dof.1989.014.01.76485.

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4

Gordeev, I. G., and E. O. Taratukhin. ""TREAT THE PATIENT, RATHER THAN THE DISEASE": MILDRONATE AS A COMPONENT OF COMPLEX CARDIOVASCULAR THERAPY." Cardiovascular Therapy and Prevention 12, no. 3 (June 20, 2013): 95–98. http://dx.doi.org/10.15829/1728-8800-2013-3-95-98.

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The paper focuses on cytoprotective and additional effects of mildronate. The emphasis is on the latest original research evidence on mildronate effects in the settings of cardiovascular and cerebral ischemia. The authors also describe the latest laboratory data on the new therapeutic potential of mildronate.

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5

Dzerve, Vilnis. "A Dose-Dependent Improvement in Exercise Tolerance in Patients With Stable Angina Treated With Mildronate: A Clinical Trial “MILSS I”." Medicina 47, no. 10 (November 5, 2011): 78. http://dx.doi.org/10.3390/medicina47100078.

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Objective. To assess the efficacy of various doses of Mildronate in combination with standard therapy for the exercise tolerance of patients with stable angina pectoris. The primary efficacy variable was the change in exercise time in bicycle ergometry from the baseline to 12 weeks of treatment. The secondary endpoints were the changes in maximum achieved load and time to the onset of angina from the baseline to week 12. Material and Methods. A total of 512 patients with chronic coronary heart disease who had ischemia as the limiting factor in the exercise test from 72 study centers in 4 countries were enrolled in this prospective, randomized, double-blind, placebo controlled phase 2 study. The patients were assigned to either 4 groups receiving standard therapy plus Mildronate at different daily doses or 1 group receiving standard therapy plus placebo. Results. The mean change in the total exercise time in the mildronate 100 mg and mildronate 300 mg groups was –2.12±108.45 and 11.48±62.03 seconds, respectively. The mean change for the placebo group was –7.10±81.78 seconds. The difference between Mildronate 100 mg and 300 mg and placebo groups was not significant. Patients in the Mildronate 1000 mg group showed a remarkable increase in the mean change in the total exercise time (35.18±53.29 seconds, P=0.002). Mildronate at a dose of 3000 mg caused a smaller increase as compared with a dose of 1000 mg. Similar changes in the secondary end parameters were observed. Conclusion. The most effective dose of Mildronate in combination with standard therapy was found to be 500 mg twice a day.

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6

Isajevs, Sergejs, Darja Isajeva, Ulrika Beitnere, Baiba Jansone, Ivars Kalvinsh, and Vija Klusa. "Mildronate as a Regulator of Protein Expression in a Rat Model of Parkinson’s Disease." Medicina 47, no. 10 (November 5, 2011): 79. http://dx.doi.org/10.3390/medicina47100079.

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Background. Mildronate (3-[2,2,2-trimethylhydrazinium] propionate dihydrate) traditionally is a well-known cardioprotective drug. However, our recent studies convincingly demonstrated its neuroprotective properties. The aim of the present study was to evaluate the influence of mildronate on the expression of proteins that are involved in the differentiation and survival of the nigrostriatal dopaminergic neurons in the rat model of Parkinson’s disease (PD). The following biomarkers were used: heat shock protein 70 (Hsp70, a molecular chaperone), glial cell line-derived nerve growth factor (GDNF, a growth factor promoting neuronal differentiation, regeneration, and survival), and neural cell adhesion molecule (NCAM). Material and Methods. PD was modeled by 6-hydroxydopamine (6-OHDA) unilateral intrastriatal injection in rats. Mildronate was administered at doses of 10, 20, and 50 mg/kg for 2 weeks intraperitoneally before 6-OHDA injection. Rat brains were dissected on day 28 after discontinuation of mildronate injections. The expression of biomarkers was assessed immunohistochemically and by Western blot assay. Results. 6-OHDA decreased the expression of Hsp70 and GDNF in the lesioned striatum and substantia nigra, whereas in mildronate-pretreated (20 and 50 mg/kg) rats, the expression of Hsp70 and GDNF was close to the control group values. NCAM expression also was decreased by 6-OHDA in the striatum and it was totally protected by mildronate at a dose of 50 mg/kg. In contrast, in the substantia nigra, 6-OHDA increased the expression of NCAM, while mildronate pretreatment (20 and 50 mg/kg) reversed the 6-OHDA-induced overexpression of NCAM close to the control values. Conclusion. The obtained data showed that mildronate was capable to regulate the expression of proteins that play a role in the homeostasis of neuro-glial processes.

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7

Sokolovska, J., J. Rumaks, N. Karajeva, D. Grinvalde, J. Sharipova, V. Klusha, I. Kalvinsh, and N. Sjakste. "The influence of mildronate on peripheral neuropathy and some characteristics of glucose and lipid metabolism in rat streptozotocin-induced diabetes mellitus model." Biomeditsinskaya Khimiya 57, no. 5 (2011): 490–500. http://dx.doi.org/10.18097/pbmc20115705490.

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Streptozotocin (STZ) was used to induce the diabetic rat model. STZ rats were treated with mildronate (100 mg/kg daily, per os or intraperitoneally for 6 weeks). Body weight, blood glucose, triglyceride, ketone body concentrations, glycated hemoglobin percent (HbA1c%), glucose tolerance, and the development of neuropathic pain were monitored throughout the experiment. In the STZ + mildronate group, mildronate treatment caused a significant decrease in mean blood glucose (on week 4) and triglyceride concentrations (on weeks 3-6), significantly slowed the increase in HbA1c% (on week 6) and improved glucose tolerance 120 minutes after glucose ingestion during oral glucose tolerance test versus the STZ group. Mildronate completely protected development of STZ-induced neuropathic pain from the first administration week up to end of the experiment. The obtained data indicate clinical usefulness of the drug for the treatment of diabetes mellitus and its complications.

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Mikhin, V. P., Yu M. Pozdnyakov, F. E. Khlebodarov, and O. N. Koltsova. "Mildronate in cardiology practice – current evidence, ongoing research, and future perspectives." Cardiovascular Therapy and Prevention 11, no. 1 (February 20, 2012): 96–103. http://dx.doi.org/10.15829/1728-8800-2012-1-96-103.

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The review discusses the benefits and various practical aspects of the new cardioprotector mildronate use in cardiology. The latest evidence on the mildronate role in complex therapy of patients with stable angina, or patients in the rehabilitation period after myocardial infarction, is summarised.

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9

Tolstov, S. N., and V. B. Mychka. "Metabolic (cytoprotective) therapy of menopausal disturbances." Cardiovascular Therapy and Prevention 10, no. 3 (June 20, 2011): 72–75. http://dx.doi.org/10.15829/1728-8800-2011-3-72-75.

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The paper presents modern views on cardiovascular aspects of menopause and metabolic therapy of menopausal disturbances with meldonium (Mildronate®). The role of estrogen deficiency in climacteric disturbance development, key pathogenetic mechanisms of menopausal metabolic syndrome (MS), and relevant features of arterial hypertension and endothelial dysfunction development are discussed. The data on Mildronate® clinical use for cardiovascular prevention are summarized. The wide prevalence and multiple clinical manifestations of menopausal disturbances point to the need for their complex therapy. Mildronate® therapy is a new approach for systemic correction of metabolic disturbances in women with climacteric symptoms and menopausal MS.

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Tolstov, S. N., V. B. Mychka, I. A. Salov, Yu V. Prokhorova, and V. A. Vyshivanyuk. "Comparative effectiveness of the approaches to correct vascular structural and functional disturbances in postmenopausal women." Cardiovascular Therapy and Prevention 11, no. 4 (August 20, 2012): 23–35. http://dx.doi.org/10.15829/1728-8800-2012-4-23-35.

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Aim.To compare the effects of Mildronate and hormone replacement therapy (HRT) with estradiol (1 mg) and drospirenone, DSPR (2 mg) on circadian blood pressure (BP) profile, arterial structure and function, and vascular stiffness parameters in women with early postmenopause and climacteric syndrome (CS).Material and methods.The study included 94 women with early postmenopause and CS, who provided written informed consent to participate and were divided into two groups. Group I included 36 women receiving Mildronate (500 mg twice a day), while Group II included 28 women who were administered, according to clinical indications, HRT (1 mg 17β-estradiol and 2 mg DRSP once a day). The control group (CG) included 30 women who did not receive either Mildronate or DRSP. At baseline and 16 weeks later, all participants underwent the assessment of blood biochemistry; intima-media thickness (IMT) of common carotid artery (CCA); endothelium-dependent vasodilatation (EDVD) of brachial artery (BA); antithrombogenic activity of vascular wall; aortal pulse wave velocity (aPWV); arterial stiffness; and 24-hour BP monitoring (BPM).Results.The study demonstrated positive effects of Mildronate therapy and HRT (1 mg 17β-estradiol and 2 mg DRSP) on metabolic status, circadian dynamics and variability (Var) of BP, and arterial structure and function. The largest positive changes in blood lipid profile were observed in Group I and II patients. By the end of the study, these patients demonstrated significantly decreased levels of systolic and diastolic BP and reduced BP Var, particularly in Group II. Mildronate therapy, but not HRT, was associated with normalisation of vascular wall antiaggregant potential. Group II demonstrated a significant reduction in CCA IMT levels, with a similar tendency in Group I. In both groups, the degree of endothelial dysfunction (ED) decreased, which was manifested in increased BA EDVD, decreased aPWV, and reduced arterial stiffness and was more pronounced in Group II.Conclusion.In menopausal women with CS, the effects of Mildronate and HRT on metabolic, structural, and functional disturbances were similar. Therefore, Mildronate therapy could be a new method of correction of these systemic disturbances.

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11

Filippova, A. V., A. P. Pereverzev, E. Yu Ebzeeva, and O. D. Ostroumova. "Mildronate. Chronic fatigue syndrome." Medical alphabet, no. 7 (June 16, 2020): 15–20. http://dx.doi.org/10.33667/2078-5631-2020-7-15-20.

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Chronic fatigue syndrome (CFS) is a state of constant, impairing quality of life, fatigue, lasting more than 6 months, inexplicable by any of coexisting patient’s pathological conditions. The prevalence of CFS in the world is approximately 2 % of the population (120–140 mln inhabitants of Earth). The etiology of CFS is unknown. Several theories of development of CFS have been proposed (immune, infectious, endocrine, metabolic, neurological, psychiatric), however, none of them fully explains the clinical manifestations of CFS. There is no specific treatment for this condition. This article presents the clinical case of a patient B 45 years old with CFS, who received treatment with regular physical exercises, diet (limiting consumption of coffee and caffeine-containing products, alcohol, salt intake to less than 5 g per day, an increase in the consumption of plant foods and products containing potassium, calcium, magnesium), as well as intake of Mildronat, a positive dynamics was observed, manifested by an increase in productivity at work, decrease in fatigue, a decrease in the daily variability of blood pressure and a decrease in heart rate at rest.

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12

Nedogoda, S. V., M. E. Statsenko, S. V. Turkina, I. A. Tyshchenko, L. V. Poletaeva, V. V. Tsoma, A. A. Ledyaeva, E. N. Chumachok, and O. L. Bykova. "Mildronate effects on cognitive function in elderly patients with arterial hypertension." Cardiovascular Therapy and Prevention 11, no. 5 (October 20, 2012): 33–38. http://dx.doi.org/10.15829/1728-8800-2012-5-33-38.

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Aim. To assess the effects of the “interval” (3 months of treatment, followed by treatment-free 3 months) and “persistent” (52 weeks) therapy with Mildronate (500 mg/d) in elderly patients with arterial hypertension (AH) and cognitive dysfunction. Material and methods. In total, 1800 elderly patients with AH and mild to moderate cognitive dysfunction were randomised into 3 groups. Group I (“interval” treatment) included 60 patients (28 men and 32 women; mean age 69,13±1,09 years), who received Mildronate 500 mg once a day in the morning for 3 months, then had a treatment-free period of 3 months, followed by 3 months of therapy and 3 months of no therapy. Group II (“persistent” treatment) included 60 patients (20 men and 40 women; mean age 73,25±2,19 years), who received Mildronate 500 mg once a day in the morning for 12 months. Group III (controls) included 60 patients (16 men and 44 women; mean age 67,75±2,05 years), who were administered only standard antihypertensive treatment. The groups were comparable by age, gender, concomitant pathology, and blood pressure levels. To assess the cognitive status at Weeks 4, 12, 26, and 52, all participants underwent neuro-psychological testing (Mini-Mental State Examination (MMSE), Schulte test, Reiten test, Wechsler test, speech, memory (memorising 10 words), and counting test). Results. In elderly patients with AH, both regimens of Mildronate treatment were significantly associated with preserved cognitive and mnestic functions, which was manifested in increased mean scores of MMSE and its time domain. However, the “interval” Mildronate treatment was more beneficial than the “persistent” therapy, as the former was also linked to a significant improvement in attention and speech MMSE domain, reduction in the time of memorising 10 words and performing Reiten test, improvement in delayed memorisation, and increased mean score in Wechsler test. Conclusion. Additional treatment with Mildronate (500 mg/d), as both “interval” and “persistent” therapy, was associated with preserved cognitive and mnestic functions in elderly AH patients.

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Vertkin, A. L., N. O. Khovasova, V. V. Pshenichnikova, M. A. Alekseev, and A. U. Abdullaeva. "MELDONIUM: EFFECTIVE ACTION POINTS." Cardiovascular Therapy and Prevention 12, no. 2 (April 20, 2013): 94–97. http://dx.doi.org/10.15829/1728-8800-2013-2-94-97.

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The paper is focused on hypoxia and cell ischemia as universal pathogenetic mechanisms of disease development, which can be addressed by both etiotropic and pathogenetic therapy. The latter is represented by the so-called metabolic correctors. At present, one of the most widely used metabolic correctors is mildronate. The authors discuss the effectiveness of mildronate in various clinical situations and also present the relevant original findings.

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Klusa, Vija, Ulrika Beitnere, Jolanta Pupure, Sergejs Isajevs, Juris Rumaks, Simons Svirskis, Zane Dzirkale, and Ivars Kalvinsh. "Mildronate and its Neuroregulatory Mechanisms: Targeting the Mitochondria, Neuroinflammation, and Protein Expression." Medicina 49, no. 7 (August 4, 2013): 47. http://dx.doi.org/10.3390/medicina49070047.

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This review for the first time summarizes the data obtained in the neuropharmacological studies of mildronate, a drug previously known as a cardioprotective agent. In different animal models of neurotoxicity and neurodegenerative diseases, we demonstrated its neuroprotecting activity. By the use of immunohistochemical methods and Western blot analysis, as well as some selected behavioral tests, the new mechanisms of mildronate have been demonstrated: a regulatory effect on mitochondrial processes and on the expression of nerve cell proteins, which are involved in cell survival, functioning, and inflammation processes. Particular attention is paid to the capability of mildronate to stimulate learning and memory and to the expression of neuronal proteins involved in synaptic plasticity and adult neurogenesis. These properties can be useful in neurological practice to protect and treat neurological disorders, particularly those associated with neurodegeneration and a decline in cognitive functions.

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Kalvinsh, I. Ya. "NEW PATHOGENETIC FACTORS OF ATHEROSCLEROSIS DEVELOPMENT AND POTENTIAL THERAPEUTIC APPROACHES." Cardiovascular Therapy and Prevention 12, no. 5 (October 20, 2013): 87–90. http://dx.doi.org/10.15829/1728-8800-2013-5-87-90.

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It has been demonstrated that one of the factors in the pathogenesis of atherosclerosis, with the subsequent development of myocardial infarction (MI), stroke (S), or sudden death (SD), is trimethylaminoxide (TMAO), the end-product of dietary choline, betaine, or carnitine metabolism by intestinal microflora. Simultaneously elevated levels of TMAO and carnitine are associated with a doubled or even tripled risk of MI, S, and SD. Therefore, dietary intake of choline-rich phosphatidylcholine fats and red meats and carnitine-rich dairy is an important risk factor (RF) of atherosclerosis. At the moment, there is no universally accepted therapeutic approach which reduces TMAO and carnitine levels. The only agent which can simultaneously reduce the levels of these two atherosclerosis-associated RFs is a well-known cardio- and cytoprotector Mildronate. Experimental and pilot clinical studies of Mildronate effectiveness in patients with obliterating atherosclerosis suggest the need for further, more detailed clinical trials of Mildronate, for estimation of its efficacy and safety.

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Jargin, Sergei V. "Meldonium (Mildronate): Primum nоn nocere." Pharmacological Research 114 (December 2016): 294. http://dx.doi.org/10.1016/j.phrs.2016.10.004.

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17

Mikhin, V. P., and O. N. Koltsova. "Mildronate effectiveness in post-hospital rehabilitation of patients with myocardial infarction." Cardiovascular Therapy and Prevention 11, no. 2 (April 20, 2012): 57–61. http://dx.doi.org/10.15829/1728-8800-2012-2-57-61.

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Aim. To study the effects of mildronate, as a component of complex therapy, on left ventricular (LV) systolic and diastolic function and exercise capacity (EC) in myocardial infarction (MI) patients undergoing post-hospital rehabilitation. Material and methods. This open, randomized study included 2 groups (50 men in each group; mean age 53,8±2,7 years): the control group (CG) and the main group (MG), which suffered MI in 4 weeks prior to the study inclusion (70% with Q-wave MI and 30% with transmural MI), and had stable post-infarction angina, Functional Class (FC) II, and ejection fraction (EF) >35%. In both groups, pharmaceutical therapy included metoprolol (75-150 mg/d), isosorbide mononitrate (40 mg/d), aspirin (100 mg/d), clopidogrel (75 mg/d), atorvastatin (20-40 mg/d), and enalapril (2,5-5 mg/d). The MG patients additionally received mildronate (1,5 g/d) for 3 months. The follow-up period was 1 year. EC was assessed using veloergometry (VEM) and 6-minute walk test (6MWT). LV systolic and diastolic function was assessed with the use of Doppler echocardiography. The following parameters were calculated: EF, DTE, LV isovolumetric relaxation time (IVRT), and enddiastolic pressure (EDP). Two types of diastolic dysfunction (DD) were defined: Type I (E/A <1; DTE >0,220 ms) and Type II (E/A >1,5; DTE <0,150 ms). Results. Mildronate therapy facilitated EC recovery, improved VEM threshold capacity, and increased 6MWT velocity and distance. In addition, mildronate improved LV systolic and diastolic function in both types of DD, by increasing EF and reducing EDP. In type I DD, E/A and IVRT increased, while DTE decreased. In Type II DD, the changes were also positive, but different: E/A decreased, while IVRT increased. Conclusion. Adding mildronate to the complex therapy of MI patients at the post-hospital rehabilitation stage facilitates EC improvement and benefits LV systolic and diastolic function.

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Rumaks, Juris, Jolanta Pupure, Simons Svirskis, Sergejs Isajevs, Gunars Duburs, Ivars Kalvinsh, and Vija Klusa. "Search for Stroke-Protecting Agents in Endothelin-1-Induced Ischemic Stroke Model in Rats." Medicina 48, no. 10 (September 1, 2012): 77. http://dx.doi.org/10.3390/medicina48100077.

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Background and Objective. Ischemic stroke may initiate a reperfusion injury leading to brain damage cascades where inflammatory mechanisms play a major role. Therefore, the necessity for the novel stroke-protecting agents whose the mechanism of action is focused on their anti-inflammatory potency is still on the agenda for drug designers. Our previous studies demonstrated that cerebrocrast (a 1,4-dihydropyridine derivative) and mildronate (a representative of the aza-butyrobetaine class) possessed considerable anti-inflammatory and neuroprotective properties in different in vitro and in vivo model systems. The present study investigated their stroke-protecting ability in an endothelin-1 (ET-1)-induced ischemic stroke model in rats. Material and Methods. Male Wistar rats were pretreated (for 7 days, per os) with cerebrocrast (0.1 mg/kg), mildronate (100 mg/kg), or their combination, followed by the intracerebral injection of ET-1. Functional and behavioral tests were carried out up to 14 days after the ET-1 injection. Ex vivo, the number of degenerated neurons and the infarction size in the cerebral cortical tissue were assessed histologically. Results. Cerebrocrast and mildronate effectively normalized ET-1-induced disturbances in neurological status, improved the muscle tone, and decreased the number of degenerated cortical cells. Both drugs also reduced the infarction size, and cerebrocrast showed at least a 2-fold higher activity than mildronate. The combination of both drugs did not cause a more pronounced effect in comparison with the action of drugs administered separately. Conclusions. The 1,4-dihydropyridine and aza-butyrobetaine structures may serve for the design of novel stroke-protecting agents to prevent severe neurological poststroke consequences.

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Ebzeeva, E. Yu, O. D. Ostroumova, and E. V. Mironova. "Efficacy and safety of Mildronate in treatment of postinfectious asthenic syndrome (clinical examples)." Medical alphabet, no. 2 (June 12, 2020): 61–66. http://dx.doi.org/10.33667/2078-5631-2020-2-61-66.

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Asthenic syndrome is a non‑specific syndrome that is often found in general medical practice in patients with various somatic pathologies both during an exacerbation of a chronic disease, and after an acute process. The leading symptoms in the clinic of asthenia are pathological weakness and fatigue. According to various researchers, they are found in 15–45 % of people. To date, there is no universally accepted definition and clear classification of this syndrome. The main pathogenetic concepts are the psychosocial, infectious‑immune theory of asthenia. The development of asthenic syndrome in patients with somatic pathology may be associated with the depletion of the functional capabilities of the nervous system due to disturbances in the blood supply to the brain, auto‑toxicity or exposure to exogenous toxic factors in bacterial, viral infections. There is no specific treatment for this condition. This article presents two clinical cases of the development of post‑infection asthenic syndrome in a 47‑year‑old patient against community‑acquired pneumonia and in a 36‑year‑old patient after an acute respiratory‑viral infection of moderate severity. In both cases, drug treatment with Mildronate was carried out with a positive trend in the form of regression of asthenia symptoms, side effects during treatment. Mildronate belongs to the class of cytoprotectors – antihypoxants, activates glycolysis and prevents impaired transport of adenosine triphosphate, providing a sufficient level of energy synthesis, which allows cells to maintain homeostasis and morphological integrity. The immunoadjuvant properties of Mildronate are very important in post‑infectious asthenic syndrome, since a violation of the immune response plays a central role in its pathogenesis. The immunoadjuvant properties of Mildronate have been discovered in a number of studies.

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Bremanis, Gunārs, and Solveiga Maļecka. "Influence of waste liquors of mildronate production on yield and quality of winter rapeseed." Proceedings of the Latvian Academy of Sciences. Section B. Natural, Exact, and Applied Sciences. 66, no. 1-2 (January 1, 2012): 36–40. http://dx.doi.org/10.2478/v10046-011-0044-y.

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Influence of waste liquors of mildronate production on yield and quality of winter rapeseed The effect of mother liquors obtained in one production stage of the popular medicinal preparation Mildronate on yield and quality of winter rape (Brassica napus L.) grown for biofuel was tested. The mother liquors contain quaterine-type compounds, which are known to stimulate growth of lupines. In the three-year study, Mildronate mother liquors were sprayed on winter rape. The yield and fat content of rape was determined. Mother liquor contains small amounts of methyl acrylate. However, this compound was not found in rapeseed, stalks and soil. Mother liquors spray had a positive effect on soil microorganisms. In the period from initiation of flowering to maximum flowering stage, spraying with mother liquors, as well as with quaterine-M and isopropanol (basic substance of mother liquor), in most cases had a low (around 10%) positive effect on rape yield and a very small impact on the fat content in rape grain. The effects differed among years, suggesting interaction with weather conditions. The determined optimal mother liquors dosages were quite wide, from 0.4 to 10 L ha-1.

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Greenblatt, H. Karl, and David J. Greenblatt. "Meldonium (Mildronate): A Performance-Enhancing Drug?" Clinical Pharmacology in Drug Development 5, no. 3 (April 29, 2016): 167–69. http://dx.doi.org/10.1002/cpdd.264.

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22

Mikhin, V. P., N. A. Volkova, S. A. Sumin, and P. A. Eremin. "MILDRONATE POTENTIAL FOR CARDIAC ARRHYTHMIA PREVENTION IN PERIOPERATIVE PERIODcardiac arrhythmias, ischemia, metabolic disturbances, cytoprotectors, antioxidants, operation-related stress, general anesthesia, Mildronate." Cardiovascular Therapy and Prevention 13, no. 1 (February 20, 2014): 27–32. http://dx.doi.org/10.15829/1728-8800-2014-1-27-32.

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Aim. To assess the effectiveness of Mildronate in the prevention of arrhythmias during the perioperative period of open cholecystectomy under intravenous multicomponent anesthesia.Material and methods. In total, 69 patients were divided into 3 groups: with concomitant coronary heart disease (CHD), with essential arterial hypertension (EAH), or without concomitant cardiovascular disease (CVD). Each group was divided into a control subgroup (total n=36) receiving conventional treatment and a main subgroup (total n=33) additionally receiving Mildronate (500 mg twice a day intravenously: 24 hour before the operation, during premedication, during early postanesthetic period, and for 2 days after the operation). Arrhythmic episodes were registered at Holter ECG monitoring for 4 days: 24 hours before the operation; 24 hours of the operation; and 48 hours after the operation. The monitoring period was divided into 6 intervals: 1 — preoperation; 2–6 hours before the operation; 3 — anesthesia start; 4 — anesthesia maintenance; 5 — anesthesia finish; and 6 — second day after the operation.Results. Cardiac arrhythmias were registered not only among patients with EAH and CHD, but also with patients without concomitant CVD.Conclusion. Mildronate therapy reduced the number of arrhythmic episodes at different stages of perioperative period, particularly in the anesthesia start, finish, and maintenance periods among patients with CHD and EAH, as well as among CVD-free patients.

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Sjakste, Nikolajs, Aleksandrs Gutcaits, and Ivars Kalvinsh. "Mildronate: An Antiischemic Drug for Neurological Indications." CNS Drug Reviews 11, no. 2 (June 7, 2006): 151–68. http://dx.doi.org/10.1111/j.1527-3458.2005.tb00267.x.

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Zvejniece, Liga, Baiba Svalbe, Marina Makrecka, Edgars Liepinsh, Ivars Kalvinsh, and Maija Dambrova. "Mildronate exerts acute anticonvulsant and antihypnotic effects." Behavioural Pharmacology 21, no. 5-6 (September 2010): 548–55. http://dx.doi.org/10.1097/fbp.0b013e32833d5a59.

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Dambrova, M. "Mildronate Cardioprotective Action through Carnitine-Lowering Effect." Trends in Cardiovascular Medicine 12, no. 6 (August 2002): 275–79. http://dx.doi.org/10.1016/s1050-1738(02)00175-5.

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Demchenko, Sergii А., Yulia А. Fedchenkova, Hanna О. Yeromina, Inna V. Herashenko, Olha H. Berdnyk, and Anatolii M. Demchenko. "The synthesis of N-(4-aryl-thiazol-2-yl)-N1-(4,5,6,7-tetrahydro-3H-azepin-2-yl)-hydrazine hydrobromides and the cardioprotective activity of (41-methoxyphenyl-thiazol-2-yl) derivative." Pharmacia 68, no. 1 (January 8, 2021): 141–46. http://dx.doi.org/10.3897/pharmacia.68.e58788.

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A novel series of N-(4-aryl-thiazol-2-yl)-N1-(4,5,6,7-tetrahydro-3Н-azepin-2-yl)-hydrazine derivatives were synthesized by interaction of equimolar quantities of substituted α-bromacetophenones with thiosemicarbazide and characterized on the basis of their elemental analyses and spectral data. Study of cardioprotective activity of the all new products in comparison to levocarnitine and its synthetic analogue mildronate were carried out. Thus, specified results indicate, N-[(41-methoxyphenyl)-thiazol-2-yl)]-N1-(4,5,6,7-tetrahydro-3Н-azepin-2-yl)-hydrazine hydrobromide was influenced deceleration of contractive response of smooth muscles to hypoxia 13.2% more effective than levocarnitine and 6.85% more effective than mildronate and were shown pronounced cardioprotective properties. Obtained data justifies further study of N-(4-aryl-thiazol-2-yl)-N1-(4,5,6,7-tetrahydro-3Н-azepin-yl)-hydrazine derivatives as new potential cardioprotective drugs for treatment of various cardiac diseases.

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Demchenko, Sergii А., Yulia А. Fedchenkova, Hanna О. Yeromina, Inna V. Herashenko, Olha H. Berdnyk, and Anatolii M. Demchenko. "The synthesis of N-(4-aryl-thiazol-2-yl)-N1-(4,5,6,7-tetrahydro-3H-azepin-2-yl)-hydrazine hydrobromides and the cardioprotective activity of (41-methoxyphenyl-thiazol-2-yl) derivative." Pharmacia 68, no. 1 (January 8, 2021): 141–46. http://dx.doi.org/10.3897/pharmacia.68.e58788.

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A novel series of N-(4-aryl-thiazol-2-yl)-N1-(4,5,6,7-tetrahydro-3Н-azepin-2-yl)-hydrazine derivatives were synthesized by interaction of equimolar quantities of substituted α-bromacetophenones with thiosemicarbazide and characterized on the basis of their elemental analyses and spectral data. Study of cardioprotective activity of the all new products in comparison to levocarnitine and its synthetic analogue mildronate were carried out. Thus, specified results indicate, N-[(41-methoxyphenyl)-thiazol-2-yl)]-N1-(4,5,6,7-tetrahydro-3Н-azepin-2-yl)-hydrazine hydrobromide was influenced deceleration of contractive response of smooth muscles to hypoxia 13.2% more effective than levocarnitine and 6.85% more effective than mildronate and were shown pronounced cardioprotective properties. Obtained data justifies further study of N-(4-aryl-thiazol-2-yl)-N1-(4,5,6,7-tetrahydro-3Н-azepin-yl)-hydrazine derivatives as new potential cardioprotective drugs for treatment of various cardiac diseases.

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28

Suprun, E. V., and M. S. Tereshchenko. "STUDY OF ENDOTHELIOPROTECTIVE ACTION OF COMBINED MEDICINE UNDER ALCOHOLIC CARDIOMYOPATHY." Актуальні проблеми сучасної медицини: Вісник Української медичної стоматологічної академії 20, no. 1 (April 9, 2020): 49–54. http://dx.doi.org/10.31718/2077-1096.20.1.49.

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At present, due to spreading of alcoholic cardiomyopathy among the able-bodied population of industrialized countries, there is an urgent need to search for new medicines possessing a strictly targeted effect, taking into account the complex mechanisms of the damaging effects produced by ethyl alcohol on the myocardium. Therefore, the combination of L-arginine and thiotriazolin (developed by “Farmatron” scientific production association) is of great clinical interest. The same is relevant for Mildronate, Mexidol and Thiotriazolin. The aim of this research was to study the endothelioprotective effect of the medicine combining L-arginine with thiotriazoline (4: 1) (Argitril) in comparison with the standard metabolites as Mildronate, Mexidol, and Thiotirazoline on the morphological and functional characteristics of endotheliocytes and ST2 level in modelled cardiomyopathy and alcohol cardiomyopathy. Alcoholic cardiomyopathy was caused by intragastric administration of 20% ethanol solution in a dose of 8 g/kg for 90 days. All animals were divided into 5 groups, 10 animals in each. All the studied substances were administered intraperitoneally for 30 days: the combined medicine (L-arginine 100 mg/ml + thiotriazolin 25 mg/ml (4:1)) - 200 mg/kg (in recalculation for L-arginine); Mildronate (Grindeks, Latvia) - 250 mg/kg; Mexidol (NPK Farmasoft, Russia) - 200 mg/kg, Thiotriazolin (Galichfarm, Ukraine) - 50 mg/kg. The control and intact groups received physiological saline. The following indicators were assessed: endothelial cell nucleus area (μm2); the density of the nuclei of endotheliocytes (as an indicator for the number of cell nuclei per 1 mm2 of myocardial tissue area) and the relative area of endotheliocytes (%), ST2 protein. The study has shown that on the 30th day after 90 days of the development of alcohol addiction, the animals were found out to have alcoholic cardiomyopathy. A significant decrease, by 32.38%, in the area of the nuclei of endotheliocytes was observed in the animals of the test group, the density of nuclei of the endotheliocytes lowered by 7% and the relative area of the nuclei of the endotheliocytes reduced by 21.89%. An increase in the concentration of ST2 protein was observed in 3.34 times compared with the intact animals that evidences the presence of endothelial dysfunction. It has been experimentally proved that the combination of L-arginine/thiotriazolin significantly exceeds the reference medicines as Mildronate, Mexidol and Thiotriazolin in terms of endothelioprotective and cardioprotective effects (effect on the area and density of nuclei of endotheliocytes; concentration of ST2 protein).

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Pavlova, N. G., E. I. Krivtsova, and N. N. Konstantinova. "The use of the drug mildronate in obstetrics." Journal of obstetrics and women's diseases 50, no. 4 (December 30, 2021): 29–33. http://dx.doi.org/10.17816/jowd95622.

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The report contains data on positive influence of mildronatum infusion (10% NaCl) on uterine-placental and fetoplacental circulation in women with chronic placental insufficiency in the third trimester of pregnancy.

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30

Mishnev, A., I. Kalvins, L. Aleksejeva, and A. Lebedev. "Structure of mildronate, its pharmaceutical salts and cocrystals." Acta Crystallographica Section A Foundations of Crystallography 67, a1 (August 22, 2011): C567. http://dx.doi.org/10.1107/s0108767311085655.

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31

Zhao, Z., J. Chen, W. Peng, X. Wang, Z. Chen, H. Tang, Y. Liang, et al. "Single- and Multiple-dose Pharmacokinetic, Safety and Tolerability Study of Mildronate Injection in Healthy Chinese Subjects Pharmacokinetic of Mildronate Injection." Drug Research 66, no. 05 (December 23, 2015): 251–56. http://dx.doi.org/10.1055/s-0035-1569297.

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32

Popova, Tamara A., Margarita V. Kustova, Gulnara Kh Khusainova, Valentina N. Perfilova, Igor I. Prokofiev, Yulia A. Smolnyakova, Ludmila E. Borodkina, Ivan N. Tyurenkov, Oleg V. Ostrovskiy, and Olga S. Vasil’eva. "Changes in the respiratory function of the heart and brain mitochondria of animals after chronic alcohol intoxication affected by a new GABA derivative." Research Results in Pharmacology 7, no. 1 (March 23, 2021): 33–40. http://dx.doi.org/10.3897/rrpharmacology.7.60469.

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Introduction: Chronic ethanol consumption leads to significant functional and structural changes in the mitochondria of the heart and brain, increasing generation of reactive oxygen species. Therefore, the search for substances, which improve the functional state of the mitochondria and, meantime, reduce the oxidative stress, is relevant. Materials and methods: 10-months-old Wistar female rats were used in the experiments. Chronic alcohol intoxication (CAI) was modelled by replacing drinking water with a 10% ethanol solution containing sucrose (50 g/L) for 24 weeks. Four groups were formed: 1 – intact animals; 2 – animals after chronic alcohol consumption; 3 – rats after CAI which were administered RSPU-260 (25 mg/kg); 4 – rats after CAI which were administered the reference drug Mildronate (50 mg/kg). The intensity of lipid peroxidation (LPO) and the rate of oxygen consumption in various metabolic states were determined. Results and discussion: Administration of the compound RSPU-260 to the animals exposed to alcohol over a long period of time resulted in an increase in both the rate of oxygen consumption (state 3) and the respiratory control ratio (RCR) of the mitochondria of heart and brain cells. The use of a GABA derivative promoted a decrease in malonic dialdehyde in the mitochondria of the heart and brain. Total SOD activity in the mitochondria of heart cells was significantly increased in the groups of rats treated with RSPU-260. In terms of efficiency, the compound RSPU-260 was comparable to the reference drug Mildronate. Conclusions: The compound RSPU-260, and the reference drug Mildronate improve mitochondrial oxidative phosphorylation in heart and brain cells, the functioning of antioxidant enzymes in animals after CAI, and can be used to correct alcoholic damage to these organs.

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Pupure, Jolanta, Sergejs Isajevs, Elina Skapare, Juris Rumaks, Simons Svirskis, Darja Svirina, Ivars Kalvinsh, and Vija Klusa. "Neuroprotective properties of mildronate, a mitochondria-targeted small molecule." Neuroscience Letters 470, no. 2 (February 2010): 100–105. http://dx.doi.org/10.1016/j.neulet.2009.12.055.

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34

Sahartova, O., V. Shatz, and I. Kalvinš. "HPLC analysis of mildronate and its analogues in plasma." Journal of Pharmaceutical and Biomedical Analysis 11, no. 10 (October 1993): 1045–47. http://dx.doi.org/10.1016/0731-7085(93)80068-c.

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35

Loca, Dagnija, Eduards Sevostjanovs, Marina Makrecka, Olga Zharkova-Malkova, Liga Berzina-Cimdina, Velta Tupureina, and Marina Sokolova. "Microencapsulation of mildronate in biodegradable and non-biodegradable polymers." Journal of Microencapsulation 31, no. 3 (October 14, 2013): 246–53. http://dx.doi.org/10.3109/02652048.2013.834992.

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36

Popov, A. L., D. D. Kolmanovich, N. R. Popova, S. S. Sorokina, O. S. Ivanova, N. N. Chukavin, A. B. Shcherbakov, T. O. Kozlova, S. A. Kalashnikova, and V. K. Ivanov. "Synthesis and biocompatibility study of ceria-mildronate nanocomposite in vitro." Nanosystems: Physics, Chemistry, Mathematics 13, no. 1 (February 27, 2022): 96–103. http://dx.doi.org/10.17586/2220-8054-2022-13-1-96-103.

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37

LATFOULLIN, Ildus A., Alla A. PODOLSKAyA, and Gennadij P. IShMOURZIN. "efficency of MILDRONATE in The acuTe period of miocardial infarcTion." Bulletin of Contemporary Clinical Medicine 2, no. 4 (2009): 23–25. http://dx.doi.org/10.20969/vskm.2009.2(4).23-25.

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38

Voita, Daina, D. Bojare, and I. Kukulis. "MILDRONATE IMPROVES CAROTID BARORECEPTOR REFLEX FUNCTION IN HUMAN HEART FAILURE." Journal of Hypertension 22, Suppl. 1 (February 2004): S195. http://dx.doi.org/10.1097/00004872-200402001-00835.

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39

Liepinsh, Edgars, Ilze Konrade, Elina Skapare, Osvalds Pugovics, Solveiga Grinberga, Janis Kuka, Ivars Kalvinsh, and Maija Dambrova. "Mildronate treatment altersγ-butyrobetaine andl-carnitine concentrations in healthy volunteers." Journal of Pharmacy and Pharmacology 63, no. 9 (July 6, 2011): 1195–201. http://dx.doi.org/10.1111/j.2042-7158.2011.01325.x.

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40

Oppedisano, Francesca, Delia Fanello, Menotti Calvani, and Cesare Indiveri. "Interaction of mildronate with the mitochondrial carnitine/acylcarnitine transport protein." Journal of Biochemical and Molecular Toxicology 22, no. 1 (2008): 8–14. http://dx.doi.org/10.1002/jbt.20208.

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41

Kuprash, Liana, Olena Kuprash, and Svetlana Gudarenko. "Metabolic cardiocytoprotectors (trimetazidine and trimethylhydrazine) in geriatrics. Short review." Issue 2 2022, no. 2 2022 (June 7, 2022): 63–70. http://dx.doi.org/10.47855/jal9020-2022-2-5.

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The review presents the clinical studies results of the effectiveness of cardiocytoprotectors, fatty acids synthesis inhibitors, trimetazidine (preductal), and trimethylhydrazine (meldonium, mildronate) in the treatment of cardiovascular disease (angina pectoris, chronic heart failure) and the central nervous system disease (dyscirculatory encephalopathy, chronic cerebral insufficiency, stroke) various ages patients. These data indicate the prospects of using these drugs in the complex therapy of cardiovascular and cerebrovascular diseases in the geriatric clinic. Keywords: metabolic cardiocytoprotectors, cardiovascular and cerebrovascular pathology, trimethylhydrazine, elderly

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42

O. S. Pashyns’ka. "Influence of vinboron on the electrical stability and electrolyte balance of the myocardium in case of experimental alcohol cardiomyopathy in rats." Bukovinian Medical Herald 17, no. 1 (65) (February 2, 2013): 85–89. http://dx.doi.org/10.24061/2413-0737.xvii.1.65.2013.21.

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In experiments on rats with experimental alcohol cardiomyopathy it has been determined that vinboron (5 mg per kg), as well as mildronate (50 mg per kg) and thiotriasoline (100 mg per kg) exerts a cardioprotective action. It is manifested by a normalization of the heart ventricular fibrillation threshold and the blood level content of Na+, K+, Mg2+ ions. Vinboron does not yield to drugs of comparison as far as value of this particular effect is concerned.

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Jaudzems, Kristaps, Janis Kuka, Aleksandrs Gutsaits, Kirils Zinovjevs, Ivars Kalvinsh, Edgars Liepinsh, Edvards Liepinsh, and Maija Dambrova. "Inhibition of carnitine acetyltransferase by mildronate, a regulator of energy metabolism." Journal of Enzyme Inhibition and Medicinal Chemistry 24, no. 6 (November 16, 2009): 1269–75. http://dx.doi.org/10.3109/14756360902829527.

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44

Bērziņš, Agris, and Andris Actiņš. "Dehydration of mildronate dihydrate: a study of structural transformations and kinetics." CrystEngComm 16, no. 19 (2014): 3926. http://dx.doi.org/10.1039/c3ce42077a.

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45

Shutenko, Zh V., D. V. Meirena, T. I. Kagan, N. I. S'yakste, and I. Ya Kalvin'sh. "Mildronate: Mechanisms of action and prospects for correction of pathologic states." Pharmaceutical Chemistry Journal 29, no. 5 (May 1995): 309–12. http://dx.doi.org/10.1007/bf02219376.

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Dzintare, Maija, Larisa Baumane, Dainuvite Meirena, Lasma Lauberte, Ivars Kalvinsh, and Nikolajs Sjakste. "Involvement of Nitric Oxide Production in the Mildronate Mechanism of Action." Pharmacology Reviews and Communications 12, no. 3 (July 1, 2002): 163–70. http://dx.doi.org/10.1080/10604450213832.

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Kuzikov, A. V., T. V. Bulko, R. A. Masamrekh, A. A. Makhova, A. I. Archakov, S. A. Usanov, E. V. Shikh, and V. V. Shumyantseva. "Analysis of mildronate effect on the catalytic activity of cytochrome Р450 3А4." Bulletin of Russian State Medical University, no. 6 (2016): 10–15. http://dx.doi.org/10.24075/brsmu.2016-06-02.

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48

Klusa, Vija, Ruta Muceniece, Sergejs Isajevs, Darja Isajeva, Ulrika Beitnere, Ilona Mandrika, Jolanta Pupure, et al. "Mildronate enhances learning/memory and changes hippocampal protein expression in trained rats." Pharmacology Biochemistry and Behavior 106 (May 2013): 68–76. http://dx.doi.org/10.1016/j.pbb.2013.03.012.

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Dambrova, Maija, and Edgars Liepinsh. "Response to comment by Sergei V. Jargin: “Meldonium (Mildronate): primum nоn nocere”." Pharmacological Research 114 (December 2016): 295–96. http://dx.doi.org/10.1016/j.phrs.2016.10.005.

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Svalbe, Baiba, Liga Zvejniece, Edijs Vavers, Osvalds Pugovics, Ruta Muceniece, Edgars Liepinsh, and Maija Dambrova. "Mildronate treatment improves functional recovery following middle cerebral artery occlusion in rats." Behavioural Brain Research 222, no. 1 (September 2011): 26–32. http://dx.doi.org/10.1016/j.bbr.2011.03.027.

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