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By Prof. Dr. R. Jacob (auth.), Prof. Dr. Rainer W. Gülch, Prof. Dr. Gerolf Kissling (eds.)

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Vial JH, Boyd GW (1989) Histometric assessment of renal arterioles during DOCA and postDOCA hypertension and hydralazine treatment in rats. J Hypertension 7:203-209 50. Weber KT, Janicki JS, ShroffSG, Pick R, Chen RM, Bashey RI (1988) Collagen remodeling of the pressure-overloaded, hypertrophied nonhuman primate myocardium. Circ Res 62:757-765 51. Weber KT (1989) Cardiac interstitium in health and disease: the fibrillar collagen network. J Am Coli Cardiol13:1637-1652 52. Wiest G (1990) Die Uingenzunahme der arteriellen GefaBe im Rattenherzen wiihrend des physiologischen Wachstums.

The treated groups were compared with nontreated SHR and normotensive WKY (n = 10 in each group). When the therapy was started in 6-month old male SHR, blood pressure was increased and left ventricular hypertrophy had developed. On the other hand, pathologic changes of myocardial structure were not observed. After 3 months, the nontreated hypertensive rats showed cardiac fibrosis (volume density of fibrosis +45% ), activation and proliferation of interstitial cells (volume density of nonvascular interstitium + 240% ), media hypertrophy of small arteries (total volume of arterial media in the left ventricle + 180% ), reduced capillarization (length density of capillaries -11% ), as well as focal degeneration of myocytes at the ultrastructural level.

Note the enhanced stroke-volume of the larger heart under otherwise almost constant contractile conditions (dashed curves). The normalization in diagram (c) is related to the smallest heart in the whole group R. w. Gulch et a!. 48 Ventricular Volume Stroke Volume Ejection Fraction Rei. Circum. Shortening Fig. 2. Transmission of circumferential shortening into stroke-volume demonstrated for a rotational ellipsoidal ventricle. The open columns correspond to a standard ventricle of volume 1, the hatched ones to a three-times larger ventricle.

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