[Chronic endometritis combination with non-inflammatory diseases of the uterine body and cervix].

The biopsies of endometrium and surgical material from 1752 pubertal, reproductive, premenopausal and menopausal age patients were investigated. Chronic endometritis was discovered in all age periods. It was suggested to distinguish the following forms of chronic endometritis: 1) an isolated form, 2) a form associated with inflammatory pathology of other parts of the genital tract, 3) a form associated with non-inflammatory diseases of the corpus and cervix of the uterus. The latter was observed considerably more frequently than other forms. Thus, non-inflammatory lesions of uterine corpus and cervix are factor of risk for development of chronic endometritis.

[The effect of nimodipine on a local ischemic brain lesion]. / Vliianie nimodipina na lokal'noe ishemicheskoe porazhenie mozga.

A modified rat model of ischemic brain injury caused by ligation of the middle cerebral artery is proposed. The time course of morphological changes in brain tissues was studied and bilateral cerebral circulatory disorders, hypoxic cortical neurocytic damages followed by intracellular regeneration, as well as metabolic and structural changes not only in the cortical neurocytes, but in the conduction paths and synaptic terminals. Nimodipine had no effect on blood supply to the ischemic brain either early or late in ischemic brain injury after ligation of the middle cerebral artery.

[Combined pathology of the pancreas and myocardium in myocardial infarction and acute destructive pancreatitis]. / Sochetannaia patologiia podzheludochnoi zhelezy i serdechnoi myshtsy pri infarkte miokarda i ostrom destruktivnom panktreatite.

Pancreas was studied in 30 patients who died of myocardial infarction (MI). Total pancreonecrosis was found in 1 case (recurring MI), diffuse focal pancreonecrosis in 3 cases (the second MI). Local microcirculation disturbances, thrombosis of some interlobular veins, degenerative changes of the exocrine pancreocytes with translocation of zymogen granules and their parapedesis into the edematous interstitium were found in all other cases. Focal metabolic myocardial damage and circulation disturbances mainly in the subendocardium of the left ventricle myocardium were found in the heart of 3 patients who died of pancreonecrosis and 60 white rats with pancreatitis induced by chloroethyl. There was a redistribution of Ca2+ in the ultrastructural components of the cardiomyocytes with its accumulation in the cytosol and sarcoplasmic reticulum. The most pronounced and widespread myocardial damage was observed in the hemorrhagic stage of pancreatitis.

[The reactivity of the links in the blood microcirculatory bed of the gallbladder in an experiment]. / Reaktivnost' zven'ev gemomikrotsirkuliatornogo rusla zhelchnogo rusla v éksperimente.

By means of TM-1 television capillaroscope morphofunctional changes of the gall bladder hemomicrocirculatory bed were studied in 40 male rabbits on the day 16 of starvation and 15 days after taking the animals on their normal ration. The data obtained demonstrated the stageness of reorganization of hemomicrocirculatory bed of serous coat of the gall bladder and indicated its high mobility and significant resistance, thus confirming the possibility of correction in exerting influence upon the organism.

[The morphofunctional changes in the hepatocytes of rats with experimental acute pancreatitis]. / Morfofunktsional'nye izmeneniia gepatotsitov u krys pri éksperimental'nom ostrom pankreatite.

Under experimental acute pancreatitis of rats, certain changes were revealed in the liver histological structure, hepatocyte population composition, intensity of hepatocyte DNA-synthesis, their proliferation, and in hepatocyte glycogen contents. These changes reflect a two-step process of hepatocyte activation. This results well compares with the earlier evidence on changes in pancreatic cell population under acute pancreatitis. The role of hepatocyte protective reactions during regenerative process in pancreas, under acute pancreatitis and its transition into chronic condition, is discussed.

[Metabolic and morphological disorders of the brain under hypokinesia and their pharmacological correction]. / Nekotorye aspekty metabolicheskikh i morfologicheskikh narushenii golovnogo mozga v usloviiakh gipokinezii i ikh farmakologicheskaia korrektsiia.

Experiments on rats have established that hypokinetic life leads to morphological and metabolic changes in tissue. Simultaneously, there is a negative dynamics in rheological and vascular changes. GABAergic substances have been found to have a tendency to level off morphological changes from 15 to 45 days of experimental investigations, but no later and they are of great energy value for brain tissue by stimulation of glucose utilization rates.

[Morphofunctional changes in the exocrine pancreatic cells in acute experimental pancreatitis in rats]. / Morfofunktsional'nye izmeneniia ékzokrinnykh pankreatsitov pri ostrom éksperimental'nom pankreatite u krys.

Experimental pancreatitis was induced by cooling the splenetic part of rat pancreas with chlorethyl, and the cells of duodenal area of the pancreas were studied at different stages of pancreatitis using cytomorphometry, cytomorphology and autoradiography. Interlobular and interacinar oedemas were observed at the first hours after treatment. In 24 hours the intracellular oedema of exocrine pancreatic cells (EP) was detected. On day 14 after treatment typical acute edematous pancreatitis developed. The observed changes involve a pathological activation of EP of the duodenal area, a subsequent restoration of the structure of this area, and later a passage of pancreatitis into the chronic form. The usefulness of this model of pancreatitis for quantitative cytochemical studies of EP during pathogenesis and drug treatment is discussed.

[Cytological research on the action of sodium thiosulfate on the process of induced acute pancreatitis in rats]. / Tsitologicheskoe issledovanie deistviia tiosul'fata natriia na protsess indutsirovannogo ostrogo pankreatita u krys.

The influence of sodium thiosulfate (STS) on the process of experimental acute pancreatitis (EAP) in rats was studied by cytomorphology, morphometry, autoradiography and cytophotometry. The influence was shown to vary at different stages of disease development. At the first stage ("primary effect" state) STS leads to the increase in the stability of exocrine pancreacytes (EP) against the toxins and to the decrease in the activity of proteases formed during necrobiosis. This results in the drop of the number of degrading EP and of the degree of inter- and intracellular oedema, and brings about shifts towards the normal values of the nucleus cytoplasm shapes, the nucleus/cytoplasm ratio, the EP population structure and their RNA and protein content. At the second stage STS stimulates DNA synthesis in EP and their proliferation leading to accelerated restoration of the number of viable cells. STS also stimulates the regeneration process hence preventing pancreatitis from passage to its chronic form. The mechanism of STS action of EP functions in normal cells and during pathogenesis is discussed.

[Changes in the content of nucleic acids and total protein in exocrine pancreatocytes and the composition of their population in experimental acute pancreatitis in rats]. / Izmenenie soderzhaniia nukleinovykh kislot i summarnogo belka v ékzokrinnykh pankreatsitakh i sostava ikh populiatsii pri éksperimental'nom ostrom pankreatite u krys.

Using cytophotometry, contents of DNA, RNA and total protein were measured in the rat's exocrine pancreatocytes (EP) in normal conditions and at different stages of pancreatitis induced by cooling the spleen part of the pancreas with chlorethyl. In the duodenal (not damaged) part of the pancreas some drastic changes in the EP ploidy distribution were shown to occur. They led to the formation of a qualitatively new population pattern with 4c and 2c + 2c cells prevailing (more than 60% of the total content), which are by 1.5-3 times more active in RNA and protein synthesis and accumulation than the normal cells. The population structure rearrangement in the EP and their functional activity rise took place at two stages. At the first one the intracellular defense mechanisms of the EP in response to acute necrobiotic processes in the pancreas tissue were activated, at the second one the supracellular mechanisms regulating synthetic processes leading to a rapid adaptation of viable EP to new conditions were switched on.

[Synthesis of mitochondrial proteins in isoproterenol-induced damage of the rat myocardium]. / Sintez mitokhondrial'nykh belkov pri izoproterenolovom povrezhdenii miokarda krys.

A rate of 14C-amino acids incorporation into mitochondrial proteins was studied during necrosis of myocardium developed after intraperitoneal injection of (-)isoproterenol to 1-, 3- and 6 months old rats. The rate of label incorporation into the outer membranes fraction was decreased in all the age groups studied, whereas incorporation of the label into the fraction of inner membranes was increased in myocardium of 1 month old rats and decreased in other age groups. Proteins of mitochondrial inner membrane were fractionated by means of electrophoresis in 10% polyacrylamide gel. In the group of 3 months old animals 23 fractions were detected, while only 18 fractions were found in 1- and 6 months old rats.

[Ribonuclease in the experimental therapy of pancreatitis]. / Ribonukleaza v éksperimental'noi terapii pankreatita.

The influence of ribonuclease on the morphogenesis of experimental pancreatitis in the albino rats has been studied. The drug injected during edematous stage of pancreatitis caused some decrease of pancreatic enzymes level in the blood at hemorrhagic stage and its normalization at necrotic stage of pancreatitis. The development of hemorrhagic and necrotic stages of pancreatitis did not change under the influence of ribonuclease. The maturation of connective tissue of pseudocyst capsule was delayed and inflammatory infiltration of necrotic tissues and their elimination were increased under the influence of the drug. There were extensive tubular transformations of acini and early fibrosis and lipomatosis in the frontier zone. In the viable parts of pancreas moderate hypertrophy of exocrine pancreatocytes developed and chronic pancreatitis features appeared with use of ribonuclease.

[Effect of synthetic analogs of L-enkephalin on viable areas of the pancreas in experimental pancreatitis]. / Vliianie sinteticheskikh analogov L-énkefalina na zhiznesposobnye otdely podzheludochnom zhelezy pri éksperimental'nom pankreatite.

Synthetic analogues of L-enkephalin--tageflar and dalargin were studied for the treatment of experimentally-induced pancreatitis of rats. It was concluded that morphometric features of an intact part of the pancreas were not significantly changed with the use of tageflar. The intensity of 14C-leucine inclusion in the proteins of an intact part of the pancreas was strongly suppressed and the cytoplasm of exocrine pancreocytes was overloaded with zymogen granules. With the use of dalargin, a moderate hypertrophy of exocrine pancreocytes and intensification of 14C-leucine inclusion developed gradually. The number and disposition of zymogen granules were not significantly changed, as compared to acute pancreatitis. Both drugs disturbed the process of acinar reconstruction into tubular complexes in the marginal areas.

[Effect of tageflar, a synthetic analog of L-enkephalin, on the morphogenesis of experimental pancreatitis]. / Vliianie sinteticheskogo analoga L-énkefalina--tageflara na morfogenez éksperimental'nogo pankreatita.

It has been substantiated that the use of a new synthetic drug tageflar analogous to L-enkephalin was accompanied by the depression in pancreatic enzyme activity in the blood of rats, acceleration of necrotic and lytic processes in irreversibly damaged exocrine pancreocytes in the course of experimental pancreatitis. The drug promoted microcirculation retention in the injury zone and acceleration of the arrangement and elimination of necrotic glandular tissue. The influence of tagaflar diminished the extent of perifocal necrobiotic zone and suppressed sclerotic processes and pancreatic lipomatosis.

[Pathological anatomy and pathogenesis of experimental pancreatitis]. / Patologicheskaia anatomiia i patogenez éksperimental'nogo pankreatita.

The necrotic and inflammatory processes in the albino rats pancreas were studied by histological, immunomorphological and electron microscopic techniques after freezing of the pancreas. Early morphological sings of acinar cells destruction were revealed. The mechanism of secret "leakage" from zimogen granules into acinar cell cytoplasm was shown. The stages of pathologic process corresponding to different types of pancreatitis were established. The inflammatory reaction formed in the stage of parenchymal necrosis was characterised by an early activation of fibroblastic and macrophagal cells and by the delay of necrotic tissue elimination with their following calcification. The chronic pancreatitis developed on the immune basis in the intact parts of the pancreas.

[Effect of sodium thiosulfate on viable areas of the pancreas in experimental pancreatitis]. / Vliianie tiosul'fata natriia na zhiznesposobnye otdely podzheludochnoi zhelezy pri éksperimental'nom pankreatite.

Experimental pancreatitis in white rats is marked by stromal edema, dystrophic changes of acinar cells, with intracellular edema in an intact part of the pancreas. Subsequently the acinar cells undergo intracellular regeneration and hypertrophy, which is accompanied by intensive incorporation of 14C-leucin into glandular proteins. Sodium thiosulfate prevents the development of stromal edema and intracellular edema of the acinar cells and retards the development of acinar cell hypertrophy. The drug produces an inhibitory action on 14C-leucin incorporation into pancreatic proteins.

[Effect of gordox on the pancreas in experimental pancreonecrosis]. / Vliianie gordoksa na podzheludochnuiu zhelezu pri éksperimental'nom pankreonekroze.

Early treatment with gordox of white rats with experimental pancreonecrosis reduces amylasemia and prevents dissemination of steatonecroses. The drug appreciably improves pancreatic microcirculation. Similarly to the control, the injured part of the gland undergoes necrosis. However, the severity of hemorrhagic component is minimal. The treatment with gordox enhances leukocytic infiltration aimed at elimination of necrotic tissues.

[Morphology of the "pancreatorenal syndrome"]. / K morfologii "pankreatorenal'nogo sindroma".

Histological and histochemical studies of the kidneys of white rats with acute pancreonecrosis have demonstrated that as a result of fermentemia and toxemia the kidneys develop a number of successive changes depending on the pattern and the intensity of the pathological process in the pancreas. A picture of the "shock" kidney was seen in the stage of hemorrhagic pancreonecrosis formation. Profound changes in the form of exudative glomerulitis, focal tubular and glomerular necrosis were seen in the kidneys in the stage of "parenchymal" necrosis. The recovery of the renal structure and function correlated with the stage of encapsulation of the necrotic focus in the pancreas.

[Changes in vascular permeability and the state of mesenteric mast cells in acute experimental pancreatitis and following treatment with sodium thiosulfate]. / Izmeneniia sosudistoi pronitsaemosti i sostoianie tuchnykh kletok bryzheiki krys pri ostrom éksperimental'nom pankreatite i pri vozdeistvii tiosul'fata natriia.

Increased vascular permeability of the mesentery was revealed in rats with experimental pancreatitis in the stage of pancreonecrosis with hemorrhagic component. This circumstance is related to a great extent to the release of biogenic amines, histamine and serotonine, from mast cells of the "microregion" and to the diminution of the amount of tissue eosinophils, an antihistamine link in the permeability control. Application of sodium thiosulfate improved vascular permeability, normalized the content of biogenic amines in mast cells and preserved the amount of eosinophils in the mesentery because of the protective effect of the drug on the pancreas.