[The nephrotoxic action of heavy crude with a high vanadium content and of its refinery products]. / Nefrotoksicheskoe deistvie tiazheloi, s vysokim soderzhaniem vanadiia nefti i produktov ee pererabotki.

The samples of vanadium-rich oil obtained from the field in Buzachi peninsula and of this oil products were applied subcutaneously to hybrid mice. In response to the application 27.5-56.6% of the animals developed renal impairment manifest morphologically in the range from acute proliferative glomerulonephritis to nephrosclerosis. Nephrotoxicity of the products increased with elevation of their sublimation temperature. Vanadium concentrations grew respectively. Intraperitoneal introduction of the products to rats provoked acute intracapillary glomerulonephritis with partial tubular and glomerular necrosis associated with acute renal failure.

[The pathogenesis of hydrocele]. / K patogenezu gidrotsele.

Hydropic fluid in hydrocele was studied for physicokinetic properties on whose basis an attempt was made to explain the pathogenetic mechanism responsible for dynamic fluid collection in the disease. A total of 45 patients with idiopathic hydrocele whose duration was an average of 4 years were examined. In the majority of cases, the disease was secondary to scrotal injuries. The authors determined hydropic fluid viscosity, hydrostatic pressure in the hydrocyst, total protein levels in the serous fluid, and intensity of hydrocyst absorption of methylene blue after its prior administration into the hydrocyst. The hydrostatic pressure in the hydrocyst, the total protein content, and the viscosity of the serous fluid were found to be directly proportional to each other. The intensity of serum methylene blue absorption was higher, its concentration being lower in most cases than in health. Thus, the pathogenesis of hydrocele seems to be as follows. In imbalance of serous fluid exudation and absorption flows as a consequence of lymphostasis and venous congestion, its collection starts in the vagina, which is accompanied by an increase in the hydrocyst's volume and an elevation of its hydrostatic pressure. With this, microcirculatory abnormalities deteriorate as a result of impaired vascular wall permeability, which causes a change in the composition of the serous fluid and an increase in its viscosity. The elevated hydrostatic pressure results in higher viscosity of the serous fluid, vice versa. Finally, this thermodynamic self-developing system will convert to a new equilibrium state with the established viscosity, pressure, temperature that ensure a balance of flows.