ВЛИЯНИЕ МЕДИКАМЕНТОЗНОЙ ТЕРАПИИ И ТИРЕОИДЭКТОМИИ НА ФУНКЦИЮ ЭНДОТЕЛИЯ И ГУАНИЛАТЦИКЛАЗНУЮ АКТИВНОСТЬ ГЛАДКОМЫШЕЧНЫХ КЛЕТОК ПЛЕЧЕВОЙ АРТЕРИИ У ПАЦИЕНТОВ С ТОКСИЧЕСКИМ ЗОБОМ | AMiner
ВЛИЯНИЕ МЕДИКАМЕНТОЗНОЙ ТЕРАПИИ И ТИРЕОИДЭКТОМИИ НА ФУНКЦИЮ ЭНДОТЕЛИЯ И ГУАНИЛАТЦИКЛАЗНУЮ АКТИВНОСТЬ ГЛАДКОМЫШЕЧНЫХ КЛЕТОК ПЛЕЧЕВОЙ АРТЕРИИ У ПАЦИЕНТОВ С ТОКСИЧЕСКИМ ЗОБОМ
Introduction. Mechanisms of change in vascular reactivity and synthetic endothelial function remain controversial in thyroid pathology. Controlled hemostasis in areas of vascular injury is one of the important functions of the endothelium. Lack of coordination between synthetic and vasomotor endothelial function may be a possible cause of increased tissue bleeding in the surgical treatment of toxic goiter. Methods. Endothelial function and guanylate cyclase activity of smooth muscle cells of the brachial artery (GCAM) were studied in a prospective observational study. 49 women aged 44 (33; 50) years were examined. Vasomotor function of the brachial artery in response to short-term ischemia (EDVD) and oral administration of nitroglycerin (ENVD), flow-induced production of endothelin-1, prostacyclin and nitric oxide were measured. The parameters were evaluated in hyperthyroidism, drug-treated hyperthyroidism and on the 4–5 day after thyroidectomy in postoperative hypothyroidism. Results. We have established the consistency of flow-induced production of nitric oxide and endothelin-1 (r = 0.78; p = 0.01) in toxic goiter. Paradoxical vasoconstriction in response to sublingual glyceryl trinitrate administration or short-term ischemia was associated with excessive level of endothelin-1 (> 0.36 fmol/ml; p = 0,05) and TSH suppression < 0.03 mIU/L (p = 0.003). The magnitude of the EDVD varied depending on the ENVD and flow-induced production of prostacyclin (R = 0.87; RI = 0.75; p = 0.00001). Deleting of the thyroid gland led to a decrease of EDVD and increase of GCAM. The relationship between the magnitude of variability of these parameters had a linear character (r = 0.66; p = 0.02). Findings. TSH suppression below 0.03 mIU/L in toxic goiter is accompanied with excessive synthetic endothelial function, which is implemented in a paradoxical vasoconstriction. Increased ability of the endothelium to synthesize prostacyclin may be a possible cause of increased tissue bleeding while removing toxic goiter.