[The effect of long-term beta-blockers on melatonin secretion, sleep quality, and vascular brain damage]. / Vliyanie dlitel'nogo priema beta-adrenoblokatorov na sekretsiyu melatonina, kachestvo sna i sosudistoe porazhenie golovnogo mozga.

Circadian rhythm of pineal melatonin production is paced by the thalamus suprachiasmatic nucleus (SCN) depending on the lighting conditions via signal transduction to pinealocytes beta-receptors. Melatonin is a natural regulator of many physiological processes, and the decrease of its synthesis leads to various diseases, in particular, insomnia and metabolic disorders. It is known that administration of beta-blockers reduces melatonin production, but the data showing clinical significance of melatonin reduction associated with beta-blockers administration are still contradictory. OBJECTIVE: The influence of long-term administration of beta-blockers to melatonin synthesis, sleep quality and vascular brain damage. MATERIALS AND METHODS: The main study group included 114 patients, aged 47-83, with cardiovascular diseases, who were under a complex therapy with long-term administration of beta-blockers. The comparison group included 110 patients with cardiovascular diseases, similar in age and sex, who did not receive beta-blockers in their complex therapy. The circadian dynamics of melatonin synthesis was observed by excretion of 6-sulfatoxymelatonin (6-SM), the major metabolite of melatonin, in three urinary samples (day, evening, night). All the patients underwent night polysomnography to assess the severity of sleep disorders. The severity of vascular brain damage was assessed using magnetic resonance imaging. RESULTS: The analyses showed large variability in individual values of 6-SM circadian excretion of patients with cardiovascular diseases (from 0.9 to 133 µg/24h with a mid-point 16.8 µg/24h). A considerable decrease of 6-SM circadian excretion is detected in the group of patients taking beta-blockers comparing to those not Me [q 25; q 75]: 12.8 [6.2; 21.1] and 24.0 [12.5; 41.5] µg/24h, respectively (p<0.001), with no differences in sleep values and severity of vascular brain damage. Comparing subgroups of patients with 6-SM circadian excretion lower and higher than 16.8 µg/24h showed a significant increase of sleep latency, decrease of rapid eye movement sleep (REM sleep), increasing number of gliosis foci in white matter of the brain with higher values of leptin, leptin/adiponectin ratio and glycohemoglobin in the group of patients with 6-SM circadian excretion ≤16.8 µg/24h. CONCLUSION: A low level of endogenous melatonin is a risk factor for development of sleep structure and quality disorders, vascular white matter brain damages with a higher risk for metabolic disorders. Long-term beta-blockers administration decrease endogenous melatonin synthesis to 50% increasing the risk for insomnia and vascular brain damage, mostly in patients with lower initial level of 6-SM circadian excretion.: melatonin, 6-sulfatoxymelatonin, beta-blockers, insomnia, vascular white matter brain damage, leptin, adiponectin.

[A role of insomnia in the development of silent cerebral infarctions]. / Rol' insomnii v razvitii nemykh infarktov mozga.

AIM: To investigate the relationship between insomnia, hemostatic abnormalities and silent cerebral infarctions. MATERIAL AND METHODS: A complex study of 76 male patients, aged 40-85, with vascular risk factors was carried out. Magnetic resonance imaging (MRI) data was used to verify presence of silent cerebral infarctions; the presence and severity of insomnia were determined using questionnaires and polysomnography. Laboratory diagnosis included a complete assessment of hemostatic system with thrombodynamics test. RESULTS: Patients were divided into 2 groups according the MRI data. The 1st group included 20 men with less than 4 silent cerebral infarctions, the 2nd group 56 men with multiple silent cerebral infarctions - from 5 to 25. Chronic insomnia was diagnosed in 35 (46%) of patients, more frequently in the second group (25% and 54% respectively, p<0.05). The group of patients with multiple silent infarctions demonstrated a loss of sleep efficiency and hypercoagulation with an increased rate of clot growth in thrombodynamics test. Correlation analysis confirmed the dependence between sleep efficiency and quantity of vascular sites, sleep efficiency and clot growth rate. CONCLUSION: The more severe plasma haemostasis disorder in patients with multiple silent infarctions and relation between insomnia severity and plasma haemostasis activation suggest that insomnia can be an additional risk factor of arteriole thrombosis.

[Reproductive Biology and a Genome Resource Bank of Felidae].

The main achievements in applying modern reproductive technologies to the banking of the genetic resources of the Felidae family are reviewed. The classification of felids at the level of species and subspecies is revised in the light of recent molecular data. Special emphasis is made on such mainstream technologies as semen collection and cryopreservation followed by artificial insemination, as well as on in vitro maturation and fertilization of oocytes combined with the culture of in vitro-derived felid embryos.

[Chronic blockade of serotonin transporter promotes restoration of the sensitivity of pulmonary vessels to vasoconstrictive agents in rats with monocrotaline-induced pulmonary hypertension].

Dose-dependent change of the reactivity of pulmonary vessels with respect to serotonin and phenylephrine were investigated in rats with monocrotaline-induced pulmonary hypertension caused by the chronic administration of fluoxetine. It was found that the treatment with fluoxetine favors a decrease of the vasoconstrictive response in pulmonary vessels. The results suggest that the chronic administration of fluoxetine can restore the reactivity of pulmonary vessels and eliminate the symptoms of pulmonary hypertension.

[Chronic administration of serotonin transporter inhibitor (fluoxetine) decreases monocrotaline-induced pulmonary hypertension in rats].

The effect of a chronic fluoxetine treatment on the development of monocrotaline-induced pulmonary hypertension has been studied in rats. It was found that fluoxetine decreased right ventricular hypertrophy and reduces pulmonary vessels thickness. These results suggest that chronic fluoxetine treatment can lead to a decrease in the manifestation of pulmonary hypertension symptoms.