Arterial hypertension in dogs with experimental informational pathology of their higher nervous activity.

It is shown that stable arterial hypertension can be formed in dogs by the development of experimental pathology of higher nervous activity (behavior) as a result of prolonged brain work during exposure to a combination of three unfavorable factors: a large volume of information to be processed and assimilated, shortage of time allowed for the work, and a high level of motivation of behavior. Three types of development of arterial hypertension were found, correlating with changes in behavior; self-regulating behavior reflecting defensive activity of the brain is particularly interesting. A high degree of self-regulating behavior was found to increase the resistance of the animal to arterial hypertension but weakening of self-regulation of behavior facilitates its onset and development.

[Arterial hypertension in dogs in a state of experimental informational pathology of higher nervous activity].

A stable arterial hypertension was obtained in dogs by means of experimental pathology of higher nervous activity (behavior) produced with a prolonged work of the brain in conditions of unfavourably combined triad of factors: large volume of information to be processed and assimilated, the factor of time set for such brain work, and a high level of behavioral motivation. Three types of arterial hypertension were revealed to correlate with the changes in behaviour. One form of this behaviour is the self-regulatory activity reflecting the defense mechanisms of the brain.

[Energy support and the contractile capacity of glycerinized myocardial fibers in experimental informational neurosis].

Experiments in dogs revealed that in informational neurosis the ability of myocardial contractile protein system (myocardial glycerinized filament bundles) to develop tension and produce work as well as the power of the contractile process are considerably reduced. Obviously, the energy production is not disturbed as a lower myocardial content of ATP (by 12%) and particularly of CP (by 54%) is caused by 8-9-month hypokinesia. Analogous shifts seem to occur in the human heart in informational neurosis which, in combination with the reduced intensity of the calcium transport by sarcoplasmic reticulum and mitochondria, may underlie the development of heart weakness.

[Catecholamine concentration and adenyl cyclase and phosphodiesterase activities of the sarcolemma of myocardial cells during hypokinesia and in experimental information neuroses].

Restriction of motor activity and motor-alimentary conditioning in dogs reduced the adrenaline (A) and noradrenaline (NA) contents in the myocardium, dopamine, too, revealing a tendency to reduction. Basal activity of the sarcolemma adenylate cyclase (AC), its sensitivity to A, NA and NaF did not change as well as the basal activity of sarcolemma phosphodiesterase (PDE) and its sensitivity to the inhibitory effect of high concentrations of Ca2 (10(-4) M). In experimental informational neurosis, NA content in the myocardium increased 5-fold compared to control values, the dopamine content also increasing.