Abstract. Introduction. Despite the abundance of methods of conservative and surgical treatment of patients with chronic arterial insufficiency (CAI) and chronic venous insufficiency (CVI) their effectiveness cannot be considered to be satisfactory since the healing of ulcers is delayed for a long time (months, years) thus remission does not exceed 2-3 years and the frequency of recurrences reaches 50–70% within 6 months. The aim of the study is to establish the features of humoral regulation of the water-salt balance in patients with trophic ulcers of the lower extremities which developed as a result of chronic arterial insufficiency and venous circulatory insufficiency. Material and methods. The main group included 115 patients with arterial foot ulcers (at the stage of critical ischemia of the arteries of the femoropopliteal segment TACSII type D, subgroup A) and 97 patients with trophic venous leg ulcers (subgroup B ‑ CVI with varicose veins C6, S, Ep, As, Ad, Po) who were examined for surgical treatment at the time of their admission to the clinic. In the comparison group ‑ subgroup A included patients with CAI TACSII of type A (n=76), subgroup B included patients with CVI C62, S, Ep, As, Po (n=63). All examined patients of the main group had ulcerative defects of Degree I-II with an area of up to 10 cm2 . The patients’ average age in the study group and the comparison group was 46.7±8.1 and 44.3±5.4 years, respectively. 25 healthy volunteers were in the control group. The criteria of exception were patients with uncontrolled hyperglycemia (HbA1c>12%), diabetes mellitus, malignant neoplasms, active necrotizing fasciitis, wounds with open joint capsules and the wounds and concomitant medical therapy such as immunosuppressants / corticosteroids. Results and discussion. There were studied the systemic and local manifestations of ischemia, the production of hormones that regulate VCB (volume of circulating blood), water-salt metabolism and inflammatory-reparative processes in the tissues of the distal lower extremities. The dualism of general and specific mechanisms was revealed. On the one hand, they were aimed at compensating for hemodynamic disturbances, and on the other, they caused the imbalance of hydrostatic and colloid-oncotic microcirculation factors. Conclusions. The pathogenetic mechanism involved in the decompensation of arterial and venous circulatory insufficiency is the imbalance of the hydrostatic component caused by the specific relationship of the hormones of the hypothalamic-pituitary-adrenal system ‑ ADH, aldosterone and cortisol and colloid-oncotic pressure. Decompensation of arterial circulatory failure is accompanied by the imbalance between ADH, aldosterone and plasma osmolarity which can be caused by an increase in the plasma content of electrolytes (potassium, chloride and calcium) and glucose, and the consequence is a disturbance of fluid filtration from the hemocapillary into the interstitium.Decompensation of venous circulatory insufficiency is accompanied by impaired resorption of fluid into the vascular bed of colloid-oncotic plasma pressure due to a decrease in the content of albumin and globulins.
critical ischemia, circulatory insufficiency, antidiuretic hormone, aldosterone, cortisol, electrolytes, transcutaneous oxygenation.
«Bulletin of problems biology and medicine» Issue 4 (162), 2021 year, 124-129 pages, index UDK 616.13/.14-005.6-008.64
