[Viral inclusions of sarcoid granuloma into the epitheliocytes]. / Virusnye vkliucheniia v épitelioidnykh kletkakh sarkoidnoi granulemy.

Electron microscopy was used study the cellular composition of sarcoid granulomas in the lung of 10 patients. In 4 patients, epithelioid cells contained herpes virus virions. In these patients, the disease clinically began acutely, ran along with erythema nodosum; their treatment involved glucocorticosteroids. In the other patients, the cells of sarcoid granulomas did not contain viruses, the granulomas were at the fibrosing stage; diffuse pneumosclerosis was clinically diagnosed. It is suggested that in sarcoidosis, immunity is of not sterile character and the phagocytosis of virus aggregates with epithelioid cells demonstrates the degree of endocytobiosis. This process takes place in tuberculosis, which is a manifestation of the biological expediency of endocytobiosis as this allows infection immunity to be maintained.

[Morphometrical assessment of the tuberculous cavern structure in tobacco smokers]. / Morfometricheskaia otsenka stroeniia stenki tuberkuleznoi kaverny u kuril'shchikov tabaka.

527 patients of the lung disease hospital filled in questionnaires. Cavernal walls of 22 patients with fibrocavernous lung tuberculosis were studied morphometrically. Among patients with tuberculosis 21.7 +/- 3.6% males and 4.05 +/- 0.8% females smoked. Total amount of tobacco smoke tars was calculated for assessment of their toxic effect. Tars "stimulate" a specific layer of granulation tissue and "inhibit" process of pneumosclerosis. Fibro-cavernous secondary tuberculosis prevails in smokers, tuberculoma and posttuberculosis pneumosclerosis are characteristic for never-smokers.

[Prevalence of tobacco smoking among phthisio-pulmonological inpatients]. / Rasprostranennost' tabakokureniia sredi patsientov ftiziopul'monologicheskogo statsionara.

A questionnaire survey of 222 phthisiopulmonological inpatients has indicated that 21.7 of the males and 4.05% of the females are smokers. Among clinical and morphological forms of tuberculosis, fibrocavernous tuberculosis is prevalent in smokers. Tuberculoma and post tuberculous fibrosis of varying severity are common in never smokers. Smokers are at high risk for lung cancer and at less risk for sarcoidosis with the equal incidence of chronic obstructive lung disease. The paper states that hospital physicians pay little attention to smoking among their patients.

[Interorgan relationships in alcoholic intoxication]. / Mezhorgannye otnosheniia pri alkogol'noi intoksikatsii.

It is suggested, on the basis of 315 necropsies of patients who died of drunkenness and alcoholism and examination of 300 rats with acute and chronic alcoholic intoxication, to distinguish an "alcoholic disease" as a separate nosological entity. The stages of this disease are drunkenness, alcoholism and alcoholic abstinence syndrome. Multiple organ pathology is characteristic for the disease with obligatory microangiopathy, alcoholic encephalo-, cardiomyo- and hepatopathy. The development of the disease follows a principle of vitium cordis at which the changes in certain organs result in the progression of pathological lesions in other organs. The course of the disease is characterized by periods of remission and exacerbation provoked either by a regular alcohol consumption or by an alcoholic abstinence syndrome. Toxic effects of alcohol, acetaldehyde and catecholamines are main factors in the pathogenesis of lesions in various organs.

[Myocardial damage and the sympatho-adrenal system in ethanol abstinence syndrome in rats]. / Povrezhdenie miokarda i simpatiko-adrenalovaia sistema pri sindrome otmeny étanola u krys.

Increase in content of II-oxycorticosteroids and in activity of dopamine-beta-hydroxylase in blood serum, decrease in concentration of adrenaline in adrenal glands with simultaneous accumulation of the catecholamine in myocardium were observed in rats after intensive alcoholization within 5 days (intragastric administration of ethanol 4-5 g/kg twice daily). In this case content of noradrenaline and its density in the catecholamine-containing nervous fibers were decreased. Ethanol abolishing, as shown by dynamics of catecholamines in heart and adrenal glands, caused an additive stimulation of the sympathoadrenal system, which reached the maximal level within a day and accomplished within 3 days after the last ethanol injection. Abolishing of ethanol led to an increase in the rate of creatine kinase elimination from isolated perfused heart and to activation of the enzyme in rat blood, which reached the maximal value within 3-7 days after the last injection of ethanol. Development of myocardium impairments correlated with accumulation of catecholamines in extraneuronal structures of heart tissue.

Morphofunctional examination of the heart in rats with the alcohol withdrawal syndrome.

Using histochemical methods, light and electron microscopy, authors examined rat heart 2-6 hours, 1, 3, and 7 days after discontinuation of forced intoxication with alcohol. At the same time, they assessed the contractile function and creatine phosphokinase (CPK) activity in the isolated perfused heart, and the development of animal destruction. Ethanol withdrawal was followed by escalation of vascular disorders in the heart, dystrophic changes in the subcellular structures, considerable polymorphism in enzyme distribution and activity, and formation of foci containing disintegrating myocytes with contractures. The contractile function was impaired and CPK release increased in the isolated heart. The changes were most marked 3 days after ethanol discontinuation to disappear after 7 days. Two to seven days after ethanol cessation, 13.1% of rats perished. Cardiac injury due to alcohol withdrawal syndrome may be one of the factors leading to the development of alcohol cardiomyopathy and a cause of sudden death in patients with documented alcohol abuse.

[Participation of catecholamines in the mechanism of heart damage during the alcohol withdrawal syndrome in rats]. / Uchastie katekholaminov v mekhanizme povrezhdeniia serdtsa pri sindrome otmeny étanola u krys.

Withdrawal syndrome in rats was induced after ethanol administration in a dose of 4-5 g/kg b. w. twice daily for 5 consecutive days. Creatine phosphokinase and lactate dehydrogenase release from the isolated heart and catecholamine distribution in the heart have been investigated in rats suffering from alcohol withdrawal syndrome. Maximum rate of enzyme release was observed on the third day of withdrawal. The density of catecholamine neurons in intact hearts and the hearts of rats sacrificed 2-6 hours, 1, 3, and 7 days after the last ethanol administration was 86, 64, 28, 7 and 38%, respectively. The area of extraneuronal catecholamine distribution accounted for 2, 19, 46, 82 and 4%. Synchronous changes observed in catecholamine distribution and the rate of enzyme release suggest that catecholamines act as a trigger of heart damage in rats with alcohol withdrawal syndrome.

[Contractile function, glucose consumption and lactate release by the isolated rat heart during different regimens of alcohol administration and after discontinuation of ethanol]. / Sokratitel'naia funktsiia, potreblenie gliukozy i vysvobozhdenie laktata izolirovannym serdtsem krys pri raznykh rezhimakh alkogolizatsii zhivotnykh i posle otmeny étanola.

Acute or chronic intoxication of rats with ethanol (intragastric administration at a dose of 8 g/kg or free-choice drinking of 10% ethanol for 3 months) produced no significant changes in contractile function, glycogen content, glucose uptake and lactate release in isolated hearts. Withdrawal syndrome simulated in rats following a short period of severe intoxication with ethanol at a dose of 4-5 g/kg twice daily has demonstrated a 15 and 28% decrease in peak systolic pressure and tension time index, respectively. In this case glucose uptake and lactate release were 2 times higher. Changes in glycogen level were observed three days after the last ethanol administration. The rats, survived after the abstinence period, revealed areas of perivascular myocardial necrosis. It is concluded that withdrawal syndrome plays an important role in pathogenesis of alcoholic cardiomyopathy.

[Alcoholic lesions of the brain]. / Alkogol'nye porazheniia golovnogo mozga.

Brains of 117 alcoholics admitted in the state of alcoholic coma or abstinence syndrome with an increase of blood pressure or development of acute psychosis were studied. The changes in the human brain were compared with those occurring in the brains of 30 rats with chronic alcoholic intoxication and formation of withdrawal syndrome. It is shown that in alcoholic coma and different manifestations of abstinence syndrome vascular and cellular changes take place, that can be attributed to the action of ethanol or its metabolites, as well as catecholamines. In the brain of the animals studied the same cellular and vascular changes were found as in the mentioned alcohol-induced manifestations in man. Progression of cephalic changes due to withdrawal syndrome is associated with more marked structural changes of the hemato-encephalic barrier.

[Pathologicoanatomic diagnosis of alcoholism]. / Patologoanatomicheskaia diagnostika alkogolizma.

Using their own and literature data the authors describe morphological alterations of the brain, heart, lungs, liver, stomach, pancreas and kidneys with the aim of the pathology diagnosis of chronic alcoholism and other types of alcoholic intoxication. The approximate diagnoses in various types of alcoholic intoxication are given as well as some rules of the pathology diagnosis coding.

[Morphology of the brain and heart in alcoholic psychoses]. / Morfologiia golovnogo mozga i serdtsa pri alkogol'nykh psikhozakh.

The authors studied the brain and heart of 40 patients (30 males and 10 females) who were hospitalized with the clinical diagnosis of alcoholic delirium, Gaye-Wernike's encephalopathy, and acute alcoholic intoxication due to chronic alcoholism. The morphological alterations in the brain and heart were as follows: compromised vascular permeability, dystrophic changes in the neurons and cardiomyocytes, proliferative reaction of microgliocytes and the development of small cardiosclerosis. Such disorders can be defined as an exacerbation of chronic alcoholic encephalopathy and cardiomyodystrophy. Alcoholic damage to the heart seems to be one of the additional factors that disrupt cerebral hemodynamics which results in hypoxia of the cerebral tissue and is accompanied by impairment of the central regulation of cardiac activity and progression of cerebral changes, i. e. the pathological process develops according to the vicious circle principle.

[Myocardium in acute and chronic experimental alcoholic intoxication]. / Miokard pri ostroi i khronicheskoi alkogol'noi intoksikatsii v éksperimente.

The myocardium of both heart ventricles in acute (AAP) and chronic (CAP) alcoholic poisoning was studied in 90 randombred rats. Functional-morphological changes typical of alcoholic cardiomyodystrophy were shown to develop in the heart in AAP and CAP. In AAP, alcoholic cardiomyodystrophy may lead to acute cardiac insufficiency and in CAP to progressive reduction of the contractile function of the heart and disturbances of conductivity in it. In AAP, however, the leading factor is the disturbance of bioenergetics as a result of toxic effect of ethanol and its metabolites on mitochondrial membranes under conditions of markedly disordered microcirculation. In CAP, along disordered microcirculation. In CAP, along with compensatory-adaptative processes in cardiomyocytes there increase the defects of the contractile apparatus, and diffuse fine-focal cardiosclerosis. This is the result of a long-term effect of ethanol and progressive hypoxia due to the affected vessels and disorders in lipid metabolism. Disorders in the function of sarcoplasmic reticulum may contribute to reduced contractile capacity of the heart.

[Experimental protection of the myocardium from anoxic damage by a weak solution of formalin]. / Zashchita miokarda slabym rastvorom formalina ot anoksicheskikh povrezhdenii v éksperimente.

Experiments on 80 noninbred rats and 135 rabbits have demonstrated for the first time the possibility of cardioplegia induction with a 0.25% formaldehyde solution. In experimental heterotopic heart transplantation, cardiac function could be restored by perfusion of donor blood within up to 3 hours after cardioplegia. This was associated with restitution of sinus rhythm and direct electrical excitability, with normalization of the intraventricular pressure (for the model described). Histological, histochemical, electron microscopic and electrophysiological studies have shown that low concentrations of formaldehyde solution inhibit myocardial energy metabolism and reversibly inhibit the enzymatic activity, preventing proteolysis and thus contributing to the preservation of heart viability.