Arteriovenous Relationships in the Pathogenesis of Encephalopathy

Abstract

The study aims at investigating the disturbance in intra- and extracranial interaction of arterial and venous vessels in stable arterial hypertension (SAH) and building a model of vascular relationships in the system: inflow – the exchange field of cerebral blood flow – outflow. Baseline data were obtained by catheterization through a probe that was wedged in the superior bulb of the internal jugular vein, where the hemodynamic and biochemical parameters of cerebral blood flow were obtained. Arterial blood was collected from the thoracic aorta. We performed the correlation and factor analyses of the relationship between the parameters of inflow and outflow to the skull in SAH patients compared with those in the control group. The identified differences led to the following conclusions: There is a loss of homeostatic control for the hemodynamic (extra- and intracerebral) and biochemical regulation in SAH; the high-energy processes of the aortic chamber (systolic and pulse pressure) spread to the bloodstream of the brain; the damping function of carotid siphons is impaired; cerebral venous stasis is formed; increased pressure in the microvascular venous network of the brain is defined; and a loss of the homeostatic control of the rheological properties of blood is defined. The loss of extracranial regulation of intracranial venous pressure in SAH leads to venous plethora of the intracerebral vessels, increasing the “booster" pressure in the microvasculature, and circulatory hypoxia of brain tissues. The consequences of these changes are metabolic and hemodynamic disturbances in energy supply for activated neurons, as well as circulatory hypoxia resulting in disturbances of the regulatory function of the nervous system and mental activity, and the development of hypertonic angioencephalopathy.

Keywords

• cerebral venous stasis
• circulatory hypoxia
• homeostatic control
• hypertonic angioencephalopathy .