Ho-Dirk Kim

Human fetal heart development after mid-term: Morphometry and ultrastructural study

A total of 44 normally developed human fetal hearts aged from 17 to 40 weeks gestation were provided for routine ultrastructural and morphometric studies. For morphometric analysis, the maximal thicknesses of the anterior, lateral and posterior wall of both ventricles and that of interventricular septum were measured and the left-to-right thickness ratios calculated. The cross-sectional areas of both ventricles in the plane of the greatest heart diameter were measured with computerized image analysis system. Data were analyzed using linear regression and one-way analysis of variance. Myofibril formation occurred by attachment of thin filaments into amorphous Z materials which were presented in sarcolemmal plaques, sarcoplasmic condensations, desmosomes and in Z lines. From these Z centers, myofibrils radiated many directions and branched and anastomosed with further development. This pattern of myofibrillar development continued throughout the whole fetal period. A transverse tubule system was clearly evident in later fetal development. It occurred by invagination of sarcolemma into myocardial cells and formation of subsarcolemmal caveolae. Mitochondria, well-developed Golgi complexes, glycogen granules and well-developed microvessels were found throughout the whole fetal period. Binucleated myocytes appeared by 32 weeks gestation and this suggests that myocyte hyperplasia may cease before birth in humans. The growth of both ventricular walls, the interventricular septum and that of both ventricular cross-sectional areas showed linear regression, and the left-to-right wall thickness ratios were nearly constant. Also, there were no differences in morphometric data between the left and right ventricles. In conclusion, development of the myocyte is an ongoing process which may be continued in the post-natal period in humans, and our statistical results do not support the theory of the right ventricular dominance during the fetal period.

Expression of intermediate filament desmin and vimentin in the human fetal heart

The intermediate filament (IF) desmin provides support for contractile machinery in muscle cells, and vimentin plays an important role in maintaining the stability of mesenchymal cells and in signal transduction. However, development of IFs in heart tissue during intrauterine life in human is not well established.

Effect of pretreatment with diltiazem on left ventricular function and intracellular calcium distribution in postischemic reperfused guinea-pig hearts.

BackgroundIt has been previously demonstrated that pretreatment with diltiazem preserves mitochondrial function during postischemic repertusion. AimThe purpose of this study was to perform cytochemical and hemodynamical assessment to confirm this demonstration. MethodsIsolated Langendorff-perfused guinea-pig hearts received 10 min of diltiazem (7.5 μM) treatment, were subjected to 10 min of global ischemia and to 20 min of repertusion. Left ventricular function was monitored by connecting a balloon to a pressure transducer. Intracellular calcium was precipitated with potassium pyroantimonate and examined with a transmission electron microscope. ResultsCompared with the control and the ischemic hearts, the diltiazem-pretreated hearts showed a significant increase in the left ventricular developed pressure (LVDP), dP/dtmax (P < 0.01), and recovery rates of the LVDP (P < 0.01 versus ischemic hearts) and dp/dtmax (P < 0.05), and a decrease in the heart rate (P < 0.01). The left ventricular end-diastolic pressure (LVEDP) and leakage of creatine kinase were not significantly different. Calcium deposits were seen along the inner aspects of the sarcolemma and t-tubule membranes, and in the mitochondria of the control hearts. The number of these deposits was considerably reduced after ischemia. They reappeared principally in the mitochondria by repertusion. In contrast, the calcium deposits reappeared along the sarcolemma, t-tubule membranes, and cell junctions, and in the mitochondria in the diltiazem-pretreated hearts. ConclusionThese results suggest that pretreatment with diltiazem may improve cardiac function during postischemic repertusion, probably in part by maintenance of sarcolemmal integrity rather than by mitochondrial buffering function.