We examined 38 patients (mean age 55.92 ± 1.56 years) with a 3-5-year history of arterial hypertension. The study showed that hypertension is accompanied by endothelial dysfunction and one of its forming factors is activation of the inflammatory response. Highly sensitive diagnostic tests can verify initiation of inflammation in preclinical manifestations. The use of nonsteroidal anti-inflammatory drugs, irrespective of the tropism to cyclooxygenase forms, alleviates manifestations of endothelial dysfunction in patients with arterial hypertension.

Using the model of lung fibrosis induced by intratracheal administration of bleomycin we studied anti-fibrotic activity of combined treatment with neuroleptic haloperidol and hyaluronidase immobilized on polyethylene oxide using electron-beam synthesis. It was shown that successive administration of immobilized hyaluronidase and the neuroleptic drug inhibits deposition of collagen fibers in the bleomycin-treated lungs. Combined treatment with the test compounds reduced swelling of the alveolar epithelium, exudation and infiltration of the alveolar interstitium and alveolar passages by inflammatory cells, and desquamation of alveolocytes into alveolar lumen, so that the alveolar-capillary membrane function was preserved.

A 6-month clinical study with active therapeutic intervention was carried out to evaluate the efficacy of moxonidine for the correction of arterial hypertension in 30 patients with metabolic syndrome. Along with the metabolic neutrality for the lipid and purine metabolism, the drug demonstrated a distinct antihypertensive effect, which against the background of pronounced sympatholytic action after 3 months of therapy tends to disappear, which can be prevented by dosage correction. It was shown that the efficacy of moxonidine in reducing insulin resistance in patients with metabolic syndrome directly depends on the severity of hypersympathicotonia manifesting in heart rate over 80 bpm at rest.