Introduction. Chronic inflammatory demyelinating polyneuropathy (CIDP) is one of the most common primary polyneuropathies. A degenerative process is the underlying cause of muscular atrophy in CIDP, while muscle strength may not fully recover in patients after pathogenesis-based treatment, thus extending the period of disability. Information about factors affecting the trophic function of muscles can be used to treat neuromuscular disorders. Study aim to examine the trophotropic properties of the study participants' blood plasma and the myoprotective effect of acetylcholine concentration equivalent to non-quantal release, using an in vitro model of the myopathy component of CIDP. Materials and methods. The study included 25 patients diagnosed with typical CIDP in accordance with the EFNS/PNS 2010 criteria. The control group consisted of 25 healthy individuals. Serum antibody levels to the nicotinic acetylcholine receptor were measured in all study participants. A method for organotypic cultivation of skeletal muscle tissue and an in vitro model of the myopathy component of CIPD were developed. The effect of the study participants' blood plasma on the growth of skeletal muscle explants in organotypic culture was assessed. Results. Patients with CIPD were found to have symmetrical sensorimotor polyneuropathy of varying severity (100%); muscle atrophy (88%), and sensory ataxia (84%). The median INCAT Overall Disability Sum Score was 2 [1; 3] for the arms and 3 [2; 5] for the legs. The median Neurological Impairment Scale (NIS) score was 17 [10; 34]. The nicotinic acetylcholine receptor antibody levels were higher in patients with CIDP (0.47 [0.31; 0.54] nmol/l) than in the control group (0.02 [0.01; 0.03] nmol/l). For the first time, a myotoxic effect of the blood plasma from patients with CIDP was observed in organotypic skeletal muscle culture. Using 1:70 and 1:100 dilutions, patient blood plasma inhibited the growth of explants by 27% (n = 120; p 0.001) and 21% (n = 120; p 0.001), respectively. This myotoxic effect removed acetylcholine at a concentration equivalent to non-quantal release (108 М). Conclusion. These results expand our understanding of skeletal muscle damage in CIPD and the role of non-quantal acetylcholine in regulating skeletal muscle growth.
Sympathetic and sensory nerve fibers regulate osteosynthesis and osteoresorption processes throughout life. Fundamental research and clinical data confirm the existence of functional interactions between neurons and bone tissue cells and indicate the catabolic and anabolic effect of sympathetic nervous system mediators on bone tissue. There is practically no information about the regulation of osteoremodeling in embryogenesis. Objective: to study the effect of norepinephrine on the growth of bone tissue explants in the embryonic period of development. The studies were performed on the bone tissue explants of 12-day old chicken embryos. Norepinephrine (10-10 M - 10-4 M), propranolol (10-10 M), atenolol (10-4 M), urapidil (10-6 M) were added to the experimental Petri dishes. Norepinephrine (10-6 M) stimulates the growth of the bone tissue explants through α1-adrenoreceptors. The osteotoxic effect of high doses of the drug is realized through β2-adrenoreceptors. Embryonic osteogenesis is regulated by norepinephrine in dose-dependent manner. Physiological effect of the substance depends on the interaction with certain types of adrenoreceptors.
Introduction. Melatonin, being a powerful endogenous antioxidant, provides healthy course of pregnancy and childbirth. Decrease of melatonin levels in blood correlates with severity of preeclampsia. Currently, melatonin is viewed as a perspective antioxidant, able to improve mother’s condition during preeclampsia and protect fetus from unfavorable intrauterine environment.The objective was to study melatonin effects on remodeling of chicken embryo heart tissue under normal conditions and under oxidative stress model.Materials and methods. The study was performed using organotypic culture of heart tissue of 10–12-day-old chicken embryos. Oxidative stress was modeled by adding epinephrine 10–4 М or homocysteine thiolactone 10–3 М to culture medium.Results. The trophotropic effects of melatonin was detected at a concentration of 10–6 M. Drug stimulated heart tissue explants’ growth on 20 %. Epinephrine showed cardiotoxic effects at concentrations of 10–4 and 10–6 М. Melatonin (10–6 М) neutralized cardiotoxic effects of epinephrine (10–4 M). Cardiotoxic effects of homocysteine thiolactone (10–3 М) preserved in presence of melatonin (10–6 М).Conclusion. During embryonic period, melatonin neutralizes cardiotoxic effects of oxidative stress caused by a high concentration of epinephrine, but not by homocysteine thiolactone.
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