[Autoregulation of cerebral blood flow in condition of experimental hepatic encephalopathy].

The linear interrelation between Systemic Arterial Blood Pressure and local Cerebral Blood Flow has been shown in experiments on rats with induced experimental hepatic encephalopathy. This is evidence of complete malfunctioning of the mechanism of Cerebral Blood Flow Autoregulation. Quantitative comparison of local Cerebral Blood Flow intensity in control and experimental (Hepatic Encephalopathy) animals has shown significant increase of the basic level of cerebral blood flow in rats with induced Hepatic Encephalopathy (p<0,05). On the basis of own and literature data the chain of developments in experimental hepatic encephalopathy was drawn: excess of Nitric Oxide because of hepatic failure can cause the cerebral vasodilatation with inadequate increase of cerebral blood flow intensity, resulting in malfunction of the cerebral blood flow autoregulation, increase of Blood Brain Barrier permeability, and penetration of toxic substances in nervous tissue. As a result of these--cognitive deficiency is developed (at the best) and hepatic coma (at the worst).

[Changes in emotional state and learning process disorders in rats with experimental hepatic encephalopathy].

Animal models of liver failure are widely used for research of morphological and functional changes and pathogenetic mechanisms of hepatic encephalopathy. Changes in learning process and emotional state of rats, which were administered intraperitoneally (Phenobarbiton 40 mg/kg/day) for five days and then subcutaneously (Acetaminophen 1000 mg/kg) are described. Behaviour of rats was studied in the "open field". Experimental animals in comparison with the control group had decreased position-finding-exploring activity although the motor activity and the fear feeling level weren't changed. The testing in the multi branch maze showed that the experimental animal's learning ability was greatly decreased--from the start platform of the maze to the nest they made more mistakes and spent more time than the control group animals, and even at the end of the maze session successful completion of task (to reach the nest) wasn't exceeding 60%.

[The models of hepatic insufficiency and encephalopathy in animals].

The majority of the investigation methods of biochemical, morphological and metabolic disorders in hepatic insufficiency and encephalopathy occurrence are inadequate in use in clinical conditions because their invasiveness frequently creates dangerous situations to the patient life and health. That's why, to characterize the mechanisms, constituting the hepatic and cerebral damages base, for testing of a new medicinal preparations, aprobation of a new theoretical and clinical hypotheses, the models of an acute and chronic hepatic insufficiency are applied on the animals, permitting to unify the age, genetic peculiarities and physiological parameters of the individuals involved in experiments, the pathology character, its severity and longevity. Homogeneity of these indexes permits to estimate molecular, structural and functional disorders, laying in the base of pathological process. We have analyzed the experimental models of hepatic insufficiency, basing on the hepatotoxins usage--acetaminophen (paracetamol), carbon tetrachloride, thioacetamide, D-galactosamine, concanavalin A, lipopolysaccharides. Every existing pharmacological model of hepatic insufficiency and encephalopathy for animals owes its own advantages and faults. The choice of a model depends on tasks of the investigation and of the animal species, involved in the procedures.