[The influence of mesenchymal stem cell transplantation time on myocardial reparation in rat experimental heart failure].

Mesenchymal stem cells (MSCs) have an ability to migrate in the organism to injured tissue to exert influence on inflammation and reparation in these regions. The aim of this study was to determine the optimal time of MSCs transplantation for myocardial reparation in rat experimental heart failure. The experiments were carried out on inbred line Wistar-Kyoto rats. Myocardial experimental infarction (EI) was induced by ligation of the left descending coronary artery. MSCs were isolated from bone marrow, cultivated in vitro and injected into the tail vein on the day of experimental infarction operation. It was shown that the time of MSCs transplantation exerted an essential influence on angiogenesis in a damaged myocardium, on ventricular dilatation and morphological structure of the scar. The best time for MSCs transplantation was determined within two days before EI, and seven days after EI. As a result, the overload of the border zone of infarct region decreased, and no features of infarction relapse were shown in the border zone.

[Mesenchymal stem cell transplantation for myocardial reparation of rat experimental heart failure]. / Terapiia éksterimental'nogo infarkta miokarda u krys s pomoshch'iu transplantatsii singennykh mezenkhimnykh stvolovykh kletok.

Mesenchymal stem cells (MSC) are resident pluripotent cells of bone marrow stroma. MSC have the ability to differentiate into osteoblasts, chondroblasts and adipocytes, neurons, glia and also into cardiomyocytes. The problem of MSC use in cell therapy of various diseases and in myocardial infarction therapy is widely discussed at present. The experiments were carried out on the inbred line Wistar--Kyoto rats. Myocardial experimental infarction (EI) was induced by left descending coronary artery ligation. MSC were isolated from bone marrow, cultivated in vitro and injected into the tail vein on the day of experimental infarction operation. It was shown that the structure of injured myocardium in experimental group significantly differed from that in control group. MSC transplantation led to inflammatory process acceleration and to increased angiogenesis in the damaged myocardium; also, live cardiomyocyte layers were detected in the scar. As a result, ventricular dilatation and overload of the border zone of infarct region decreased, no features of infarction relapse were shown in the border zone.

[Elevated expression of argentophilic proteins from the nucleolar organizer regions in myocardium of patients with obstructive hypertrophic cardiomyopathy and mutations in p53 tumor suppressor gene]. / Povyshennaia ékspressiia argentofil'nykh belkov oblastei iadryshkovogo organizatora v miokarde bol'nykh obstruktivnoi gipertroficheskoi kardiomiopatiei i mutatsii v gene opukholevogo supressora p53.

Silver staining for nucleolar proteins was used to evaluate the ribosomal genes activity in cardiomyocytes (Cm) and fibroblast-like cells (FBS) of intraventricular septum, and other regions of the left ventricle. Specimens to be analysed were taken from 7 patients with idiopathic obstructive hypertrophic cardiomyopathy (OHCM). In this group the quantity of nucleoli and AgNORs, reflecting the transcriptional and processing level of pre-ribosomal RNA in all type of cells, was at least 2 and 3 times higher than in patients with essential hypertension and in healthy control, respectively. We suggest that nucleolar hypertrophy in patients with hypertrophic cardiomyopathies, inappropriate to hypertrophy in other pathological conditions, may be most probably of compensatory character, and this may be in part explained by nuclear hyperploidy and chromosomal endoreduplication. We have noted a marked heterogeneity in shape, size and quantity of nucleoli, and in AgNORs of FBC. Nuclei with modulated phenotype containing nucleoli of high activity were revealed. This article presents the first data on p53 mutation identification in patients with advanced OHCM.

AgNORs in cardiomyocytes from surgical patients with coronary heart disease.

AIM: To evaluate the interphase ribosomal RNA cistron activity of cardiomyocytes in surgical patients with chronic ischaemic heart disease by means of the nucleolar organiser region silver staining (AgNOR) technique. METHODS: Nucleoli were investigated in myocardial samples obtained from 46 patients with chronic ischaemic heart disease before, during, and soon after cardioplegia ischaemia. Cryostat sections of 10 microns thickness were air dried, fixed in methanol/glacial acetic acid (3:1) for 15 minutes, rinsed carefully with distilled water, incubated in 2 N formic acid for 10 minutes, and impregnated with silver colloid solution for 2.5-3 minutes at 68-70 degrees C. The lightly counterstained sections were examined under oil immersion at x1000 magnification. For the estimation of AgNOR numbers at least 100 silver stained cardiomyocyte and fibroblast nuclei were counted in each section. On the basis of these data, the mean number of AgNORs in each nucleus was determined. The Student's t test was used to compare the groups tested. RESULTS: The initial mean numbers of AgNORs varied greatly, demonstrating a difference between groups of patients with or without antecedent myocardial infarction (9.5 v 11.0; p < 0.05). During myocardial arrest, the numbers of AgNORs in cardiomyocytes were decreased in all but seven patients, while those in fibroblasts tended to increase. At the stage of reperfusion and myocardial warming, in all but three patients the numbers of AgNORs in cardiomyocytes either normalised or were even higher than the initial value. CONCLUSIONS: The AgNOR count in cardiomyocytes is a very sensitive test for the measurement of cardiac function in surgical patients with chronic ischaemic heart disease and could be useful for monitoring myocardial status during the course of surgery, including cardioplegia. The high risk group for surgery included patients with antecedent myocardial infarction and severe heart failure. It is thought that a reversible nucleolin/fibrillarin/pre-rRNA/small nucleolar RNA modification might account for this fast decline then rise in the AgNOR count in cardiomyocytes at the stages of cardioplegia and reperfusion, respectively.

[Cardiac involvement in diphtheria today in adults]. / Porazhenie serdtsa pri sovremennoi difterii u vzroslykh.

Postmortem morphological examination of 102 cases with diphtheria who had died on the disease day 1-120 was performed. All the dead patients were adults. Dystrophic-necrotic processes in cardiac conduction and intramural nervous systems, in contractile myocardium developing on the disease day 1-8 were found. The severity and extent of these processes depended on toxic and hypoxic factors resultant from obturation or ventilation respiratory failure. Myocarditis progression undergoes 2 stages: early, exudative (beginning on the disease day 3) and late, productive (beginning on the disease day 9). The disease eventuated in myocardiosclerosis starting after 28-day course. Morphologically, diphtheritic cardiac lesion differed from cardiac damage caused by other acute infections.

[Hyperlipidemia as a factor of myocardial damage (experimental study)]. / Giperlipidemiia kak faktor povrezhdeniia miokarda (éksperimental'noe issledovanie).

To elucidate the assumed direct negative effect of huperlipidemia (HL) on the myocardium, histological and electron microscopic studies of the myocardia of rabbits with alimentary hypercholesterolemia which were on an atherogenic diet for 30 days and underwent transesophageal pacing tests were conducted. An experimental group comprised 7 rabbits with HL, a control one included 4 animals. In HL rabbits, the cardiac pacing test caused irreversible myocardial histomorphological changes. In normolipidemic rabbits this caused only myocardial functional overload and histological changes were moderate and reversible. The findings suggest that HL contributes to myocardial hypoxic damage due to impaired microcirculation and tissue diffusion of oxygen with higher myocardial oxygen demand.

[An evaluation of the plastic function of the cardiomyocytes by silver staining of the nucleoli in patients operated on for ischemic heart disease]. / Otsenka plasticheskoi funktsii kardiomiotsitov metodom serebreniia iadryshek u operiruemykh bol'nykh ishemicheskoi bolezn'iu serdtsa.

Examinations of plastic function changes in myocardial cells (MC) from 36 patients with chronic ischemic heart disease were carried out before, during and soon after cardioplegic ischemia. The initial mean number of silver grains in nucleoli varied greatly showing some difference between groups of the patients with (9.5 +/- 0.48) or without (11.0 +/- 0.5) myocardial infarction. During the myocardial arrest this index of MC plastic activity was decreased in all but 7 patients. In contrast to this, it was elevated in most patients tested during subsequent reperfusion. On the basis of these data and parallel histochemical photometric assessment of DNA, RNA and succinate dehydrogenase activity, a hypothesis was suggested which explains the non-standard elevation of ribosomal cistron activity during both myocardial arrest and reperfusion by their compensatory reaction to myocardial injury.

[Activity of the nucleolar organizers in cardiomyocytes of patients with arterial hypertension of varying genesis]. / Aktivnost' iadryshkovykh organizatorov v kardiomiotsitakh bol'nykh s arterial'noi gipertenziei razlichnogo geneza.

A comparative study of the myocyte nucleolar organizer activity (NOA) was performed on silver-stained myocardium from 6 patients who had died from the hypertension disease and 7 others patients with secondary renal hypertension non-complicated by severe coronary atherosclerosis and heart failure. In the first group, positive correlations between NOA of cardiac cells and the level of maximal diastolic pressure (r = 0.8, p less than 0.028), wall thickness of the left ventricle (r = 0.8, p less than 0.028) as well as myocardial weight (r = 1.0, p less than 0.001) were found. In the second group, on the contrary, there was a pronounced negative correlation between NOA of the myocytes and myocardial weight (r = -0.86, p less than 0.005) which may be explained partially by a primary metabolic myocardial deficiency in such patients.

[Orthostatic hypotension in primary amyloidosis]. / Ortostaticheskaia gipotoniia pri pervichnom amiloidoze.

Proceeding from clinicoanatomical observation of a 50-year-old man, the authors discuss the pathogenesis of arterial hypotension developing in generalized amyloidosis with severe affection of the cardiovascular and nervous system, and the adrenal glands.

[Characteristics of myocardial hypertrophy in arterial hypertension of various origins and in atherosclerosis]. / Osobennosti gipertrofii miokarda pri arterial'noi gipertenzii razlichnogo geneza i ateroskleroze.

Sets of conventional macroscopic and up-to-date histochemical techniques were employed to study hearts from 267 patients who had died of essential hypertension, atherosclerosis or secondary renal hypertension. Excessive cardiac mass was found disease-specific and related to the time since hypertension onset. Cardiac hypertrophy was augmenting with growing deficiency of coronary blood supply and showed specific correlation between cardiomyocyte nucleus and cytoplasm within each nosological unit mentioned. This may serve evidence for the absence of a common morphofunctional underground for this process. Essential hypertension is characterized by stepwise nuclear changes in cardiomyocytes relevant to advancing hypertrophy.

[2 cases of temporal arteritis]. / Dva sluchaia visochnogo arterita.

Two cases of temporal arteritis are described. In patient K., aged 79 years, the disease ran an acute course and resulted in bilateral blindness. In patient T., aged 67 years, the disease ran a subacute course with a unilateral amaurosis and involvement into the disease of the cerebellar, humeral, renal, leg and, possibly, heart arteries. Elevation of the amount of circulating immune complexes in patient K. and no elevation in patient T, with the complement content being within normal, can be viewed as features of the disease progress.

[Stereological characteristics and enzymatic activity of myocardial capillaries in different variants of pathology and death (data from immediate autopsies)]. / Stereologicheskaia kharakteristika i fermentativnaia aktivnost' kapilliarov miokarda pri nekotorykh variantakh patologii i smerti (po materialam srochnykh vskrytii).

Parallel stereo- and cytospectrophotometric examinations of human myocardial capillaries, 20-60 min after biological death were carried out. The activity of alkaline phosphatase, adenosine triphosphatase, lactate dehydrogenase and NAD-diaphorase in the capillary wall in relation to the sex and age in cardiovascular pathology, renal diseases and leukemias were studied. The permeability and level of energy supply of transendothelial transport were found to depend on the kind of the main pathological process and type of death. According to the parameters under study, the functional state of the capillary network of the myocardium in atherosclerosis with or without its combination with hypertension and also in secondary renal hypertension is described.

[Quantitative histoenzymological and biochemical studies of the stages of atherogenesis in human coronary arteries (based on the data of early autopsies]. / Kolichestvennoe gistoénzimologicheskoe i biokhimicheskoe issledovanie étapov aterogeneza v koronarnykh arteriiakh cheloveka (po matarialam rannikh vskrytii).

Histochemical methods were used to study the dynamics of activity of energetic metabolism enzymes (EME) in cell elements of the human coronary artery (CA) wall in comparison with biochemical values of lipid metabolism in the plasma. The development of CA atherosclerosis was shown to be determined to a large extent by reciprocal relations of antiatherogenic alpha-lipoproteins and atherogenic beta-lipoproteins in their influence on EME activity. An increased EME activity at early stages of atherogenesis (lipid plaque) is an adaptation to changed homeostasis. The lipid plaque is a turning point in the process of metabolic adaptation. Evolution of atherosclerotic changes is accompanied by disjunction and transformation of correlative connections between EME activity in CA wall cells.