Vasomotor activity of the major and cerebral arteries was studied in mice with chronic obstructive pulmonary disease. Regional differences were revealed in the endothelium-dependent response of arteries. The development of chronic obstructive pulmonary disease was associated with a paradoxical response of the dilatational component of vasoregulation against the background of increased constrictive influences of the vascular endothelium in the major and cerebral vessels.

We studied vasomotor activity of rat cerebral vessels. Peculiarities of endothelium-dependent reactions of cerebral arteries in induced arterial hypertension were revealed. Quantitative and qualitative relationships between the parameters of the vasomotor apparatus of cerebral arteries and parameters of circulatory homeostasis were determined.

The effects of histochrome and mexidol on the morphology and function of the brain and behavior were studied in senescence-accelerated OXYS and Wistar rats. MRI showed that signs of neurodegenerative changes were present in OXYS rats at the age of 3 months and were pronounced at the age of 12 months. Histochrome (1 mg/kg, 5 days) more effectively than mexidol (4 mg/kg, 7 days) reduced anxiety and increased exploratory activity of 1-year-old OXYS rats. Both drugs improved the morphology and function of the brain. Their effects consisting in correction of diffuse changes in the white matter and reduction of edema were comparable; in addition, histochrome reduced the intensity of demyelinization processes.

Literature data of chronic obstructive pulmonary disease (COPD) and cerebrovascular diseases (CVD) comorbidity are represented in this review. Key aspects of this interaction and its importance for clinical medicine have been considered. CVD and COPD are the main mortality factors in adults, which contribute to great economic wastes. The incidence of chronic cerebral ischemia for COPD patients is almost three times as high as for general population. The incidence of ischemic stroke for COPD patients is 1,2 times higher than in general population. For hemorrhagic stroke and subarachnoid haemorrhages, this figures are 1,3 and 1,46 respectively. Chronic systemic inflammation, tissue hypoxia and oxidative stress play the crucial role in respiratory and cerebrovascular comorbidity. Metabolites of these processes (especially proinflammatory cytokines, reactive oxygen species, C-reactive protein and some neurotrophins) increase the permeability of blood-brain barrier, destroy brain cells and activate atherogenesis in pre - and intracerebral arteries. Endothelial dysfunction affects autoregulation of cerebral circulation. Systemic symptoms of COPD are closely associated with different structural-functional disorders of the brain such as reduction in white matter integrity, grey matter volume reduction and cerebral microbleeds. Also, venous encephalopathy is developed as a result of intrathoracic pressure elevation and stasis in superior vena cava system. These processes result in neurological symptomatology. The intensity of symptoms depends on COPD severity. The occurrence of cognitive impairment, psychic tension, depression, panic disorders also increases. However COPD and CVD comorbidity is an important problem of modern medicine, pathophysiologic mechanisms and clinic aspects of this problem remain unresolved. Understanding of their role opens perspectives for rational pharmacotherapy.

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