Abstract
Summary. A model of chronic obstructive pulmonary disease (COPD) was reproduced in rats by intermittent inhalation of nitrogen dioxide for 60 days. Pulmonary vascular disorders were assessed by perfusion scintigraphy and measuring pulmonary artery smooth muscle reactivity under exposure of vasodilators. Disorders of pulmonary capillary blood flow occurred at early stages of COPD (15 days) and extended not only to segments but to lobes at 60 day of exposure. Dilatability of pulmonary arteries reduced that led to reduction of the smooth muscle relaxation amplitude in response to vasodilators with different mechanisms of action. Starting from 30th day, rats were given angioprotectors (rosuvastatin and sulodexide) to treat vascular disorders. Rosuvastatin did not improve pulmonary microcirculation and pulmonary artery smooth muscle reactivity. Administration of sulodexide resulted in improvement of pulmonary microcirculation with recruitment of reserve areas. Dilatable component of the pulmonary arteries increased leading to enhanced smooth muscle relaxation in response to isoproterenol and especially to nitrosorbide. So, we could assume sulodexide-dependent recovery of NO-dependent mechanism of pulmonary artery smooth muscle relaxation and partial restoration of β-adrenergic vasodilatation.
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