MYOCARDIAL HYPERTROPHY IN MACACA-FASCICULARIS - STRUCTURAL REMODELING OF THE COLLAGEN MATRIX

  • 1 June 1987
    • journal article
    • research article
    • Vol. 56  (6) , 676-683
Abstract
The collagen skeleton in the myocardium of 37 non-human primates (Macaca fascicularis) was studied by scanning electron microscopy. Twenty-one hypertensive animals had "pressure-overload" myocardial hypertrophy of 4 to 80 weeks duration induced by unilateral perinephric cellophane insertion and 16 were normotensive controls. The purpose of the study was to examine possible remodeling of the collagen matrix of the hypertrophied pressure overloaded M. fascicularis myocardium. An extensive collagen matrix was demonstrated in nonoperated macaques, consisting of a weave which sequestered groups of myocytes and which was joined to the epimysium by long collagen tendons, and of numerous intermyocyte and myocyte to capillary struts. In addition, strands of collagen were seen crossing interfascicular planes. This collagen skeleton was studied at three periods of perinephritis-induced hypertension with hypertrophy: at 4 weeks (evolutionary); at 32 weeks with mild to moderate hypertension (early compensatory); and at 80 weeks with moderately severe hypertension (late compensatory). These sequential studies revealed that the matrix was remodeled. At 4 weeks there was slight thickening and increase in density of the weave. At 32 weeks, in addition to changes in the weave, the collagen strands became thick and pillar-like and the tendons increased in numbers and thickness, and at 80 weeks some myocytes became encased in collagen. The geometrical arrangement of the normal collagen natrix of the myocardium is similar to series and parallel elastic elements with respect to myocytes, and, accordingly, it may be responsible for the mechanical properties of the myocardium during diastole and systole. The structural alterations in the collagen skeleton which we observed in hypertrophy may play a significant role in deleteriously affecting ventricular function of the pressure-overloaded myocardium.