Beta-blockers and thimidine-3H captation in the human foetal heart.

In the present research the effects that the beta-blockers may express on the development of foetal myocardium have been studied "in vivo" and "in vitro". On the basis of previous researches (7), the beta-blocker effects have been observed by utilizing low doses in comparison with the therapeutic levels. Wistar rats affected by a surgically elicited renal hypertension and "in vitro" cultivated human heart buds, represent the two models utilized for our research. In the first model the low dose of beta-blocker, able to reduce the plasmatic renin activity (PRA) but unable to determine normal conditions of blood pressure, evokes an eccentric dilation of ventricular room and severe alterations of the myofilament pattern. Also in human heart buds cultivated in presence of beta-blocker at low levels of concentration in the cultural media, deep changes in the structural and ultrastructural pictures of the myocardium can be observed; the major changes consist in a particular and constant accumulation of glycogen in the cytoplasm of the myoblasts whose organules are pushed to the periphery of the cells. At electron microscopic level, disorders affecting the myofilaments and their genesis are present, while the intercellular junctions seem to be blocked in their ability to transfer into functional contacts; in fact, they appear only as mechanical junctions. Utilizing an autoradiographic technique the above described alterations seem to derive from a different degree of captation of thimidine-methyl-3H that appears to be higher in the specimens exposed to high dose of beta-blocker. Finally, all the results obtained seem to indicate the negative influence that the studied drugs can express on the histogenesis and the metabolism of myocardial cells.