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Diabetic cardiomyopathy is the leading cause of mortality in type 1 diabetes. Thus study of cardiomyocyte morphology and function during early stages of diabetes using modern analytical methods is of critical importance. Therefore, using confocal microscopy, we determined metric parameters, volumes and contractility, with calcium transients in isolated left-ventricular myocytes at one week after induction of diabetes in rats. Myocyte volume analysis from 3D confocal scans was performed using an automated contour detection algorithm that took the actual shape of the myocytes into account. We showed a significant reduction in myocyte volume in diabetic animals. We also showed a significant reduction in length and width but not in thickness of the myocytes, which suggests disproportional reorganization of the structure of the heart tissue during short-term diabetes. From a functional point of view, we observed a significant decrease in cell shortening at a stimulation frequency of 0.5 Hz. This was accompanied by a decrease in calcium transient amplitude. Together, these data suggest that impaired calcium handling is one of the factors that contributes to the observed decrease in myocyte shortening during early stages of streptozotocin-induced diabetes in rats. [ABSTRACT FROM AUTHOR]

To evaluate differences in tissue composition between hearts with pressure overload hypertrophy and normal hearts of comparable weight, 30 rat hearts with aortic constriction of 4, 10 and 30 days, and nine hearts of sham operated controls were studied. Surgery was performed at age 70 days. Morphometric analysis of myocardial tissue sections revealed (1) myocyte hypertrophy in left ventricular myocardium of hypertrophic hearts was proportional to heart weight, and in normal growth myocyte volume increased in proportion to heart weight; (2) myocyte number in left ventricular myocardium was identical in hypertrophic and normal hearts; (3) non-muscle cell proliferation was proportional to heart weight identically in hypertrophic and normal hearts; (4) volume fractions of myocytes were significantly lower in hypertrophic hearts [0.76(SD 0.05)] than in normal hearts [0.82(0.04)]; (5) volume fractions of all nuclei, myocyte nuclei and non-myocyte nuclei were similar in hypertrophic and normal hearts; (6) measured ventricular DNA content increased with heart weight identically in hypertrophic and normal hearts, and equalled DNA content calculated using the data on tissue composition. Neither right ventricular weight nor right ventricular DNA content were affected by the presence of left ventricular hypertrophy.We conclude that left ventricular hypertrophy due to aortic constriction in the rat resulted in changes of myocardial tissue composition similar to the changes associated with normal growth. Tissue composition of hypertrophic rat hearts corresponds strikingly to that of normal rat hearts with comparable heart weight, although myocardial changes in hypertrophy develop considerably faster than in normal growth. [ABSTRACT FROM PUBLISHER]

To obtain quantitative information on changes in myocyte size in hearts with increased myocardial mass light microscopical morphometry was used in fixed and stained myocardial tissue sections. A modification of the azan staining procedure made longitudinal (sarcolemma) and transverse (intercalated discs) boundaries visible with a contrast that allowed morphometric analysis. The method was validated in left ventricular tissue of rats ranging in age from 4 to 17 weeks. Myocyte width, cut surface area, length, and volume were significantly correlated with left ventricular weight with residual errors of 5%, 5%, 6%, and 8% respectively. The method was applied to 21 human hearts, nine of which had left ventricular hypertrophy. Myocyte width, area, length, and volume both in subepicardial and subendocardial left ventricular tissue were significantly greater in hypertrophic than in normal hearts. Although the mean weight of the hypertrophic hearts exceeded that of normal hearts by 40%, myocyte volumes in subepicardial and subendocardial left ventricular tissue of hypertrophic hearts were higher by 78% and 43% respectively, indicating a transmural difference in the extent of myocyte hypertrophy. The method is accurate and reproducible and gives useful quantitative information on changes in myocyte dimensions during normal cardiac growth as well as in cardiac hypertrophy. [ABSTRACT FROM PUBLISHER]

Myocardial DNA concentration and ventricular weight were measured in the hearts of normal and spontaneously hypertensive rats varying in age from 1 day to 1 year and the ventricular DNA content calculated. A linear relation between ventricular DNA content and ventricular weight was observed in both rat strains. This linear relation was deduced theoretically, assuming that the number of ventricular non-myocytes per heart was proportional to ventricular weight and that the number of ventricular myocytes per heart was constant after the first postnatal week. The fit with experimental data produced values of the number of ventricular myocytes (42.5 × 106) and non-myocytes (199 × 106 per gram of ventricular tissue) in normal rat heart. Using published data on ventricular volume occupied by myocytes (80%) and myocardial specific density (1.06 g·ml−1), the mean(SD) volume of individual myocytes could be calculated (17758(2632) multiplied by ventricular weight, expressed in μm3·g). The values obtained compared well with experimental observations reported in the present study (18504(131) μm3·g) and in other studies. Hearts from spontaneously hypertensive rats had lower numbers of myocytes (37.4 × 106) and non-myocytes (180 × 106 per gram) per heart than normal hearts with identical ventricular weights. Hearts of normal 2 month old rats that were made hypertrophic by various means were identical to non-hypertrophic hearts of normal older rats with identical ventricular weights in relation to the number of ventricular myocytes and non-myocytes per heart. It is concluded that ventricular hypertrophy induced in young adult rats might be regarded as normal growth occurring at an accelerated rate. [ABSTRACT FROM PUBLISHER]