GENERATION OF NEW INTERCELLULAR-JUNCTIONS BETWEEN CARDIOCYTES - A POSSIBLE MECHANISM COMPENSATING FOR MECHANICAL OVERLOAD IN THE HYPERTROPHIED HUMAN ADULT MYOCARDIUM

Citation
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
Citations number
41
Categorie Soggetti
Hematology,"Cardiac & Cardiovascular System
Journal title
ISSN journal
00097330
Volume
78
Issue
3
Year of publication
1996
Pages
362 - 370
Database
ISI
SICI code
0009-7330(1996)78:3<362:GONIBC>2.0.ZU;2-G
Abstract
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.