Activation Of Sympathetic-adrenal System Research Articles

State Of Purine Exchange And Microalbuminuria In Patients With Metabolic Syndrome

The aim of the given work was study interactions of impairments sympa-thetic – adrenal systems functional condition and processes of peroxidal oxida-tion of lipids in woman with metabolic syndrome. 107women at the age of 25-49 were observation. They were randomized into 3 groups: I (control) – 15 healthy persons, II – 43 patients with arterial hypertension, III – 49 women with arterial hypertension in combination with metabolic syndrome. The results of carried investigations showed that activation of sympathetic adrenal system and processes of peroxidal oxidation of lipids took place in metabolic syn-drome. Marked lowering of sympathetic – adrenal system key ferment catechol-amins (MAO monoaminooxidaze) desamidization activity and considerable ac-tivation of peroxidal oxidation of lipid products which have great significance in revealing the mechanism of metabolic syndrome development were observed in metabolic syndrome. This results in the prolonged toxic influence of catechola-mins on myocardium.

Autonomic support of the activity in children with small cardiac abnormalities

The aim of the study was to investigate vegetative maintenance (VM) in children with small cardiac abnormalities (SCA) using a wedge-orthostatic test (WOT). The article describes the research results of 170 children with SCA. VM was estimated with clinic orthostatic test (COT). The group of patients consisted of 106 children with mitral valve prolapse (MVP) and 64 children with false tendons (FT) in the left cardiac ventricular. We used absolute and relative statistical methods with Microsoft Excel program for this study. We found out that hypersympathycotonic type of VM was prevalent at MVP (57,6%). For FT it was only 37,5%. Pathologic type of VM with insufficient activation of sympathetic adrenal system was noted only in 21,2% of patients with SCA. This species is more common with FT (23.4%) than with MVP (19.8%). Hyper diastolic type was present only in 9,4% patients with MVP and in 3,1% with FT, respectively. Mixed types were rare noted at SCA without specification for MVP or FT (4.7% for MVP and 3.2% for FT). Thus, the revealed types of COT show the disorder of VM, which characterizes the reducing of adaptive capacity in such children.

To the noradrenergic component of the mechanisms of stress-limiting and healing effects of dalargin

The article presents the facts of the stress-limiting and healing effects of a synthetic analogue of leucine-enkefalin dalargin (D), the analysis of literature data of the modulating effects of D on the activity of sympathetic-adrenal system (SAS) in various extraordinary influences. D prevents: hyperactivity of SAS, associated development of dystrophic-destructive changes in the organs (heart, gastric mucosa, duodenum) and the exhaustion of catecholamine’s (CA) depot in the sympathetic endings. It is noted that similar protective effects against the development of neurogenic lesions in the organs (heart, gastric mucosa, liver and pancreas) have pharmacological agents with antiadrenergic component of actions (gangliolitiks and sympatholitiks, alpha - and beta-adrenoblokers). In the article mapped the healing effects of D in relation to the gastric mucosa destructions, skin incisional wounds, bone fractures with the ability of the sympathetic nervous system to stimulate reparative regeneration in various tissues (cornea. gastric mucosa, myocardium, liver, sympathetic reinnervation). It is concluded that the stress-limiting and healing effects of D have a noradrenergic component associated with modulating effect of D on the activity of SAS. In the conditions of extraordinary influences D suppresses SAS hyperactivity, keeping the reserves of CA in the sympathetic endings. In the implementation of reparative regeneration of tissues CA, and primarily sympathetic mediator noradrenalin, promote healing of damaged organs and tissues.

Regulating effect of sympathetic-adrenal system on hemopoiesis suppressed by cytostatic drugs

The ability of cytostatics to cause activation of sympathetic-adrenal system (SAS) assumes alongside their direct cytotoxic effect, the existence of mediated action on hemopoiesis, through the autonomic nervous system (ANS). Nevertheless, the possibility of sympathetic-adrenal modulation of a myelopoiesis inhibiting effect of cytostatic drugs and, in particular, 5-fluorouracil (5-FU) and cyclophosphamide (CP) has not been studied. We have established the two-phase decrease of catecholamines (CA) concentration in adrenal glands of mice on the first 2 days and on days 4 and 5 after high dose (114 mg/kg) of 5-FU injection. It was conditioned, more likely, by not a gland damage, but mediators' rejection to blood. A direct correlation is found, between CA concentration in adrenal glands and cellularity of various hemopoiesis lineages that testifies to a close dependence of the postcytostatic hypoplasia and hemopoiesis restoration on the SAS regulating effect. Using pharmacologic agents such as α-(dihydroergotaminum, 3.9 mg/kg) and β-adrenergic antagonist (propranolol, 5 mg/kg) or ganglionic antagonist (azamethonium bromide, 6 mg/kg) showed positive and negative effects on hemopoiesis regeneration of the first and second phases of CA secretion from adrenal glands, respectively. One of the drugs injected on the third day after 5-FU administration in contrast to a combined with cytostatic use, allowed enhancement of the rate and amplitude of erythro- and granulocytopoiesis restoration to a considerable degree. A similar effect of the same medicines was observed in conditions of CP administration. One of the mechanisms of modulating CA effect on hemopoiesis inhibited by cytostatics is a control of the proliferation and differentiation processes of hematopoietic cells in hemopoietic islets (HI). Thus, the processes of postcytostatic hypoplasia and restoration of hemopoiesis are determined, probably, by a combination of specific cytostatic damages of hematopoietic cells and elements of their microenvironment with non-specific SAS activation which is capable of enhancing the cytotoxic influence of cytostatics on hemopoiesis.