Objective: Cardiac hypertrophy due to a prolonged functional activity is associated with an increase of cell size and polyploidization of the myocyte nuclei. Myocardial infarction is characterized by loss of myocytes. Increased load and as a consequence hypertrophic growth of the surviving myocardium has to be expected. The aim of this study was to investigate the response of cardiomyocytes after infarction. Method: Biochemical and cytophotometric analysis was performed on myocyte and connective tissue nuclei to determine whether the human heart after myocardial infarction is accompanied by an increase in the ploidy level, DNA content and in the number of nuclei. A total of 15 hearts obtained from autopsy material was studied, among them 8 after myocardial infarction. The number of nuclei was measured by indirect computation. Results: We found a decrease of 4c and no significant difference of 2c nuclei in infarcted hearts.Ž . DNA ploidy level ) 8c as well as the proportion of aneuploid myocyte nuclei were increased in infarcted hearts. DNA concentration and total DNA content were increased in the hearts after myocardial infarction. Numerical ratio of connective tissue nucleirmyocyte nuclei, total number of nuclei, number of myocyte nuclei and number of connective tissue nuclei were increased in infarcted hearts. Conclusion: Polyploidization and nuclear hyperplasia of myocytes may represent an adaptive response of the myocardium to an ischemic injury. q 1997 Elsevier Science B.V.
DNA content, ploidy level, cell size and nuclear number were investigated in 54 mammalian hearts from nine species. DNA content was determined biochemically and ploidy level of cells was studied by the means of Feulgen cytophotometry. Nuclear number was calculated by a new method, while cell size was determined by using ocular micrometry. In most mammals diploid cell nuclei predominate. Higher ploidy levels were found in the human and the pig hearts. The total amount of DNA correlated with the myocardial weight. Eight million heart muscle cell nuclei were found in mice (myocardial weight 160 mg), and 2600 million heart muscle cell nuclei in the human heart (myocardial weight 210 g), but in the hearts of horses up to 35000 million heart muscle cell nuclei (myocardial weight 3.4 kg) were found. The number of heart muscle and connective tissue cell nuclei was correlated with myocardial weight. The ratio of connective tissue cell nuclei to heart muscle cell nuclei was between 2:1 and 3:1. In cardiac growth this ratio shifted towards connective tissue cell nuclei. Increased heart weight corresponds to an increase in cell size. Diameter between 11 microns and 18 microns may be an optimum for heart muscle cells of mammals.
The aim of our study was to correlate MRI with histologic findings in normal and degenerative cartilage. Twenty-two human knees derived from patients undergoing amputation were examined with 1.0- and 1. 5-T MR imaging units. Firstly, we optimized two fat-suppressed 3D gradient-echo sequences. In this pilot study two knees were examined with fast imaging with steady precession (FISP) sequences and fast low-angle shot (FLASH, SPGR) sequence by varying the flip angles (40, 60, 90 degrees) and combining each flip angle with different echo time (7, 10 or 11, 20 ms). We chose the sequences with the best visual contrast between the cartilage layers and the best measured contrast-to-noise ratio between cartilage and bone marrow. Therefore, we used a 3D FLASH fat-saturated sequence (TR/TE/flip angle = 50/11 ms/40 degrees) and a 3D FISP fat-saturated sequence (TR/TE/flip angle = 40/10 ms/40 degrees) for cartilage imaging in 22 human knees. The images were obtained at various angles of the patellar cartilage in relation to the main magnetic field (0, 55, 90 degrees). The MR appearances were classified into five categories: normal, intracartilaginous signal changes, diffuse thinning (cartilage thickness < 3 mm), superficial erosions, and cartilage ulcers. After imaging, the knees were examined macroscopically and photographed. In addition, we performed histologic studies using light microscopy with several different stainings, polarization, and dark field microscopy as well as electron microscopy. The structural characteristics with the cartilage lesions were correlated with the MR findings. We identified a hyperintense superficial zone in the MR image which did not correlate to the histologically identifiable superficial zone. The second lamina was hypointense on MRI and correlated to the bulk of the radial zone. The third (or deep) cartilage lamina in the MR image seemed to represent the combination of the lowest portion of the radial zone and the calcified cartilage. The width of the hypointense second zone correlated weakly to the accumulation of proteoglycans in the radial zone. The trilaminar MRI appearance of the cartilage was only visible when the cartilage was thicker than 2 mm. In cartilage degeneration, we found either a diffuse thinning of all layers or circumscribed lesions ("cartilage ulcer") of these cartilage layers in the MR images. Early cartilage degeneration was indicated by a signal loss in the superficial zone, correlating to the histologically proven damage of proteoglycans in the transitional and radial zone along with destruction of the superficial zone. We found a strong effect of cartilage rotation in the main magnetic field, too. A rotation of the cartilage structures caused considerable variation in the signal intensity of the second lamina. Cartilage segments in a 55 degreesangle to the magnetic main field had a homogeneous appearance, not a trilaminar appearance. The signal behavior of hyaline articular cartilage does not reflect the laminar histologic structure. Osteoarthrosis and cartilage de...
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