Pathogenesis of myocardial fibrosis in spontaneously hypertensive rats (SHR).

The pathomechanisms of myocardial fibrosis are incompletely understood. Coronary microvessels (MV), interstitial reactions and focal myocardial lesions characterized by morphological signs of ischaemia were found in 39 spontaneous hypertensive rats (SHR) and 33 control rats aged 3, 13, 27, 52 and 78 weeks, using new morphological preparations and measuring methods. In the developing phase of spontaneous hypertension (SH) the numerical and area densities (developed for up to 13 weeks) of MV were lower than at 3 weeks and lower than control. The same was true for the fibrotic tissue density. However, all values were increased in the manifest phase of SH (27-78 weeks). The increase in interstitial tissue is topologically and causally related to pathological MV reactions that represent morphologically chronically increased contractions. Small MV that mostly elude detection with conventional staining methods are of particular importance. The first phase of manifest SH (27th-52nd week) is characterized by a generalized development of myocardial fibrosis; the late phase (52nd-78th week) by a reinforced localized fibrosis that is attributable to the enhanced progression of focal ischaemic myocardial lesions. The septal region is not included in this phase. Thus, in the two phases of manifest SH, the pathomechanisms responsible for the development of myocardial fibrosis must be different.