EXTRACEREBRAL ZINC-DEPENDENT DISORDERS AND THEIR CORRECTION IN PATIENTS WITH ACUTE CEREBRAL INSUFFICIENCY

Introduction: zinc metabolism disorders, which often accompany the development of a critical state, may lead to numerous heterogeneous metabolic and functional disorders, both in the nervous system and in the other body systems. Objective: to improve intensive care of patients with acute cerebral insufficiency by correcting extracerebral disorders associated with zinc deficiency. Materials and methods: a clinical randomized cohort study included 94 patients aged 18 years with acute cerebral insufficiency. The concentrations of zinc, thiol compounds, intestinal fatty-acid-binding proteins, and interleukin-1β were analyzed. The dynamic changes of these indicators, their relationships with each other, depending on the underlying pathology and the medical correction of zinc sulphate monohydrate and acetylcysteine, were evaluated. Results and discussion: there was a decrease in zinc and thiol compounds serum level in the examined patients that indicates an impairment of transport zinc regulation and antioxidant defence, an increase in the level of intestinal fatty-acid-binding proteins that is a marker of gastrointestinal damage of the mucous membrane of the tract. These changes, as well as the concentration of interleukin-1β, are interrelated and depend on the zinc concentration. The exogenous introduction of zinc sulphate monohydrate and acetylcysteine promotes the normalization of the parameters studied. Conclusions: Patients with acute cerebral insufficiency have extracerebral disorders in the content of thiol compounds, as well as the disorders of the gastrointestinal mucous membrane and pro-inflammatory response. The exogenous introduction of zinc sulphate monohydrate and acetylcysteine contribute to eliminating such disorders.

Ambient temperature impact on hepatocellular liver damage in rats following intake of 3,4-methylenedioxymethamphetamine

Bacground/Aim. 3,4-methylendioxymethamphetamine (MDMA, Ecstasy) is a psycho-stimulating agent. It is usualy taken orally in the form of tablets. It is absorbed throught the gastrointestinal mucous membrane. Hyperthermia is the most prominent clinical sign of MDMA intake. The most prominent forensic finding of lethal MDMA poisoning is myocardial infarction and cerebrovascular bleeding. However, liver and kidney damage: have also been described. The aim of this research was to determine if ambient temperatures affect liver damage in the experimental rats. Methods. The experiment was conducted for 8 h and 24 h, at temperatures of 12?C, 22?C and 32?C. Both biochemical parameters (ALT, AST, AP, gamma GT and LDH) and pathohistological changes of the liver were monitored. Results. Our reserch demonstrated that the most serious lever damage occurred at 32?C. Liver damage was manifested as portal inflammation, periportal necrosis, lobular necrosis, stasis, intralobular hemorrhage and incerease of liver enzymes serum activity. Conclusion. Liver damage after MDMA intake rises with the increase of ambient temperature, and it is most pronounced at the temperature of 32?C.