[The mechanisms of disorders in the hemostatic system of patients with chronic diffuse liver diseases]. / Mekhanizmy narushenii sistemy gemostaza u bol'nykh khronicheskimi diffuznymi zabolevaniiami pecheni.

A total of 70 patients with chronic hepatitis and 60 with liver cirrhosis (LC) were examined. The hemorrhagic syndrome (HS) was identified in 16% of patients with chronic active hepatitis, in 26% with compensated and in 76% with decompensated LC. Intravital study of intravascular blood coagulation and liver microcirculation with the aid of fibrin determination according to D. D. Zerbino made it possible to establish local intravascular coagulation (LIC-syndrome). Study into the hemostatic and fibrinolytic systems, analysis of liver function, hemocoagulation and the intensity of the LIC-syndrome permitted one to arrive at conclusions about complex impairments of the hemostatic system in patients with chronic diffuse liver diseases characterized by a tendency towards blood hypocoagulation in the systemic blood flow with the risk of the development of the HS and a tendency towards hypercoagulation (with the risk of thrombosis development) in the vascular bed of the liver. It has been shown that the main cause of the HS occurring in chronic diffuse liver diseases lies in derangements of the thrombocytic component of the hemostatic system: thrombocytopenia as a consequence of hypersplenism and consumption of the most active thrombocytes in the process of the LIC. Activated fibrinolysis starts to exert an inhibitory action on hemocoagulation in patients with chronic diffuse liver diseases in the stage of decompensated LC. In compensated hepatopathies, the influence of fibrinolysis on coagulation and the development of the HS was immaterial.

[Ultrastructural pathology of the liver in abdominal typhoid]. / Ul'trastrukturnaia patologiia pecheni pri briushnom tife.

Light and electron microscopies were applied to examine liver punctates from 10 patients with typhoid fever. Both in the full swing of the disease and in clinical recovery (convalescence), dystrophic and necrobiotic changes along with focal cell death were found to occur in the hepatocytes, endothelial and Kupffer cells covering the sinuses. The protein-synthesizing system and mitochondria were demonstrated to be primarily destroyed. The microbes of typhoid fever were located in the hepatocytes, endothelial and Kupffer cells.

[Morphofunctional characteristics of changes in the exocrine portion of the pancreas in alimentary obesity]. / Morfofunktional'naia kharakteristika izmenenii vneshnesekretornogo otdela podzheludochnoi zhelezy pri alimentarnom ozhirenii.

Changes in the morpho-functional state and intracellular regeneration of the exocrinous part of the pancreatic gland in alimentary obesity were studied experimentally in rats. Systematic alimentary overloading of the pancreatic gland was found to lead to working hypertrophy of its "reserve" parts predominantly which are represented in females by tail parts of the gland and in males by the head. It is suggested that the lower regeneratory potential of the acinary cells and their greater predisposition to degenerative, necrobiotic, and necrotic changes with the progress of obesity in males may be due to greater intensity of organ vascular pathology in them and greater sensitivity of acinary cells to metabolic disorders.