Teriv P. S., Shkurupiу D. A.

Zinc-Dependent Effects during Intensive Care in Patients with Neurological Disorders


About the author:

Teriv P. S., Shkurupiу D. A.

Heading:

LITERATURE REVIEWS

Type of article:

Scentific article

Annotation:

The review of the literature considered zinc dysmetabolism and its consequences in patients with neurological disorders in the intensive care unit. Patients with severe brain affection requiring long term care in the intensive care unit. Patients with cerebral insufficiency have common systemic reactions leading to overlay of unaffected areas of brain tissue to the pathological process. This exasperates the pathological cascade of reactions which leads to affecting other organs. Patients with neurological disorders often suffer from gastrointestinal insufficiency, which prevents providing adequate nutritional support and enhances existing immune reactions as a result of bacterial translocation which in its turn leads to sepsis pathway. Motor and secretory disorders of the gastrointestinal tract lead to increasing intra-abdominal pressure, which affects the venous blood flow and furthers brain neoplasm, forming a vicious circle. In such circumstances tissues require a number of substances, including zinc at its already existing deficit. Zinc is a part of over 200 enzymes involved in the transmission of nerve impulses and synthesis of biological substances. Zinc is part of many regulators of transcription and biosynthesis of nucleic acids, it provides cells proliferation and differentiation processes. Zinc accelerates regeneration of intestinal canal mucin layer, is an important factor in maintaining the balance between cellular and humoral immunity, it stabilizes cell permeability and permeability of intracellular membranes, is an apoptosis inhibitor. Zinc was proved to be an antioxidant. Vesicular fraction of neuronal zinc escaping to a synaptic cleft at electrical simulation models activity of various receptors at synaptic transmission and prevents affecting blood-brain barrier structures. One of the early signs of zinc insufficiency is decreasing serum activity of alkaline phosphatase and carbonic anhydrase. Consequently, such patients begin suffering from stress GIT ulcers. Patients with gastrointestinal insufficiency have pathological keratinization and enterocytes degeneration with apoptosis activation. Patients with diarrhea syndrome under these conditions occur in a vicious circle between diarrhea and the level of zinc: diarrhea leads to loss of specific zinc transporters. In this case, cell detritus, microflora and undigested food bind zinc, reducing its bioavailability. Hyper-catabolism and insufficient nutritional support lead to the loss of muscle tissue with high zinc content, evolving hypoalbuminemia which prevents zinc absorption in the gastrointestinal tract. Against this background, the deficiency of this micro element is manifested by a number of clinical manifestations incl. – with the nervous system. Thus, patients in critical conditions with cerebral insufficiency have all the reasons for the formation of zinc insufficiency and caused by this factor secondary affects. Understanding these processes grounds the tactics of optimization zinc-dependent reactions in neuro-intensive care for treatment and prevention of deep life-support dysfunction.

Tags:

Zinc, neurological disorders, intensive care.

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Publication of the article:

«Bulletin of problems biology and medicine» Issue 2 part 3 (109), 2014 year, 48-52 pages, index UDK 616. 8:01/09