GENERATION OF NEW INTERCELLULAR-JUNCTIONS BETWEEN CARDIOCYTES - A POSSIBLE MECHANISM COMPENSATING FOR MECHANICAL OVERLOAD IN THE HYPERTROPHIED HUMAN ADULT MYOCARDIUM
S. Yamamoto et al., GENERATION OF NEW INTERCELLULAR-JUNCTIONS BETWEEN CARDIOCYTES - A POSSIBLE MECHANISM COMPENSATING FOR MECHANICAL OVERLOAD IN THE HYPERTROPHIED HUMAN ADULT MYOCARDIUM, Circulation research, 78(3), 1996, pp. 362-370
Intercellular dehiscence is a common cardiocytic response to pathologi
cal conditions. However, little consideration has been given to the po
ssibility of new intercellular junctions developing between cardiocyte
s within developed myocardium. To examine this possibility as it may r
elate to useful compensation for hemodynamic overloads, changes in car
diocytic connection were evaluated by scanning electron microscopy in
hypertrophied myocardium of adult human hearts. Transmural myocardium
of left ventricle was obtained at autopsy from five hearts with concen
tric hypertrophy, five hearts with eccentric hypertrophy, and five con
trol hearts (noncardiac death). After formalin fixation, the number of
cardiocytes connected to an individual cardiocyte was counted in tiss
ues from the middle portion of the transmural samples by scanning elec
tron microscopy. Cardiocytic diameter and connective tissue volume fra
ction were measured an the transmual sections by light microscopy. In
concentrically hypertrophied hearts presenting both increased cardiocy
tic diameter and connective tissue volume fraction, the number of othe
r cardiocytes connected to an individual cardiocyte (4.60 +/- 0.10 [me
an +/- SE]) was significantly increased (P<.05) compared with control
hearts (4.19 +/- 0.12) or eccentrically hypertrophied hearts (4.11 +/-
0.10). The increase in junctions per cardiocyte in concentrically hyp
ertrophied hearts suggests that new connections had been generated. Mo
re junctions developing during hypertrophy could add another structura
l advantage to those of cardiocytic hypertrophy and connective tissue
proliferation as compensatory adjustments to hemodynamic overload in c
oncentrically hypertrophied hearts.