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In order to clarify the role of the central nervous system in the genesis of arterial hypertension (AH) a population analysis of somatic pathology in schizophrenia was performed. Using clinical and postmortem data, the study found lower frequency of AH among mental patients vs. somatic ones; primary AH was benign independently of the psychotropic therapy regimen. II to III stage AH in psychosis was associated with primary or secondary renal pathology or magistral vessel atherosclerosis. Severe schizophrenia and a pronounced personality defect were associated with low intensity of the primary form of somatic nosology.

The aim of the study was to examine changes in vasodilatory endothelial function in early cerebrovascular disease of atherosclerotic genesis. All the examinees underwent ultrasonic investigation, test for reactive hyperemia of the brachial artery to evaluate vasodilatory function of the endothelium. Disturbances in the flow-dependent vasodilation were detected at initial stages of the disease, aggravated with the progress of cerebrovascular disease and therefore could serve the earliest, objective indicator of atherosclerotic process.

Central and cerebral hemodynamics was studied using echocardiography and transcranial dopplerography in 200 poststroke patients over 60 in the course of 5-year follow-up. It was established that cardiac hypodynamic syndrome, i.e. continuous or paroxysmal fall of minute blood volume below 3 l, is the most significant contributing factor in the onset of cerebral ischemia. Drugs are recommended for prevention of ischemic stroke. Those lowering cardiac hemodynamic reserve should be excluded in patients at high risk of acute failure of cerebral circulation.

Combined estimation of signs of cerebral circulatory disorders, the state of microcirculation and a degree of CHD was done in 111 male patients after myocardial infarction. Disorders in the system of the terminal bed which corresponded to the severity of clinical manifestations of disorders of coronary and cerebral circulation, were revealed in the overwhelming majority of the patients. The most noticeable changes in the terminal blood flow were observed in patients with marked clinical signs of atherosclerosis of the cerebral vessels. They also had a more severe course of postinfarction cardiosclerosis. Since noticeable microcirculatory disorders were detected in all these patients, it could be assumed that they were suggestive of the presence and severity of atherosclerosis. Symptoms of CNS lesion developed against this background and depended on the features of cerebral circulation and some other factors.