Dilated cardiomyopathy (DCM) is characterized by enlargement and dilation of all heart compartments associated with serious decrease of its contractile function. DCM hallmark is the combination of dystrophic and hypertrophic alterations of cardiomyocytes. Since the power output of cardiac cells is directly related to remodeling of their contractile machinery we investigated expression of selected contractile and cytoskeletal proteins in the left ventricle of DCM patients using immunoblotting. The content of the recognized protein markers of cardiomyocyte hypertrophy such as tubulin, desmin and slow skeletal myosin heavy chain isoform, MHCbeta, was significantly elevated in DCM compared to normal myocardium. In addition, marked increase in the content of several smooth muscle proteins (smooth muscle alpha-actin, Myosin Light Chain Kinase, Kinase Related protein SM22) that are normally expressed in embryonic myocardium, was observed in DCM hearts. Thus, cardiomyocyte hypertrophy in DCM is associated with activation of embryonic protein expression program and smooth muscle proteins could serve as markers of this process. Understanding their involvement in sarcomere assembly and pathways of their expression activation during cardiac hypertrophy may bring new insights in treatment of various forms of cardiomyopathy.

Saphenous vein segments taken at coronary bypass surgery from 34 patients (31 men and 3 women, mean 50,1+/-7,7 years) with chronic heart failure NYHA functional class I - III due to ischemic heart disease were studied histologically after staining with hematoxylin eosin. Structural parameters of the heart were obtained by echocardiography. Increase in severity of heart failure was accompanied by significant augmentation of relative vessel wall thickness mainly at the account of its muscular coat. Indexes of relative thickness of media in investigated vessels were 0,29+/-0,10, 0,48+/-0,18 and 0,61+/-0,45 in patients with NYHA classes I, II, and III, respectively. This index correlated closely with thicknesses of left ventricular posterior wall (r=0,60, p<0,01) and intraventricular septum (r=0,68, p<0,001). Thus progression of heart failure was accompanied by remodeling of peripheral blood vessels and the process of remodeling involved simultaneously muscular layer of the vessel wall and the myocardium.

The pancreas from bovine fetuses of 27-35 cm crown-rump length were used as a source of islet cell cultures. Pancreatic tissue was treated by collagenase, filtered through the metal sieve and incubated in MEM for 24 h. Using this method, cultures similar to so-called pseudo-islets were obtained. Aldehyde-fuchsin staining and electron microscopy revealed a significant number of beta-cells within the pseudo-islets, the insulin-producing activity of which was confirmed by RIA.

Ultrastructural changes in normal and hypertrophied dog hearts under conditions of total ischemia were studied by electron microscope method. In the control group sings of irreversible damage appeared in 90 min, in the presence of phosphocreatine, 10 mM, these changes became apparent in 120 min. In the hypertrophied hearts signs of the irreversible damages became evident in 60 and 90 min in the absence and presence of phosphocreatine, respectively. Ability of phosphocreatine to protect both normal and hypertrophied myocardium allows to use it safely.

Alterations in the heart energy metabolism, early defects in cardiomyocyte sarcolemma and heart resistance to ischemic damage have been investigated in experimental autoimmune cardiomyopathy. Systolic and diastolic pressures were registered and the speed of ischemic contracture development was determined on the isolated perfused rat hearts. Oxidative phosphorylation parameters, macroenergetic phosphate levels were determined. The ultrastructure and cell membrane permeability to lanthanum were studied. The results obtained have shown that the hearts of rats with autoimmune cardiomyopathy revealed decreased macroenergetic phosphate levels: ATP level was 22% lower and Pcr was 45% lower. Resistance of cardiomyopathic hearts to ischemic stress significantly reduced, cell membrane permeability was distorted. The above changes are believed to be due to incompetent myocardial hypertrophy and Ca overload.

The authors present for the first time a complete picture of ultrastructural changes of contractile cardiomyocytes in myocardial calcium necroses in the time course from reversible to irreversible stages. Three types of calcium cell lesions are singled out: rigor, lytic, and vacuolar.