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1 Departamento de Clínica Médica, Faculdade de Medicina de Botucatu, Universidade Estadual Paulista, Botucatu, São Paulo, Brazil 18618-000; and 2 Department of Anatomy, Physiology, and Pharmacology, Auburn University, Auburn, Alabama 36849-5517
We investigated the influence of myocardial collagen
volume fraction (CVF, %) and hydroxyproline concentration (µg/mg) on rat papillary muscle function. Collagen excess was obtained in 10 rats
with unilateral renal ischemia for 5 wk followed by 3-wk treatment with
ramipril (20 mg · kg
1 · day1) (RHTR
rats; CVF = 3.83 ± 0.80, hydroxyproline = 3.79 ± 0.50). Collagen degradation was induced by double infusion of oxidized glutathione (GSSG rats; CVF = 2.45 ± 0.52, hydroxyproline = 2.85 ± 0.18). Nine untreated rats were used
as controls (CFV = 3.04 ± 0.58, hydroxyproline = 3.21 ± 0.30). Active stiffness (AS;
g · cm2 · %Lmax1)
and myocyte cross-sectional area (MA; µm2) were increased
in the GSSG rats compared with controls [AS 5.86 vs. 3.96 (P < 0.05); MA 363 ± 59 vs. 305 ± 28 (P < 0.05)]. In GSSG and RHTR groups the passive
tension-length curves were shifted downwards, indicating decreased
passive stiffness, and upwards, indicating increased passive stiffness,
respectively. Decreased collagen content induced by GSSG is related to
myocyte hypertrophy, decreased passive stiffness, and increased AS, and
increased collagen concentration causes myocardial diastolic
dysfunction with no effect on systolic function.
renovascular hypertension; fibrosis; oxidized glutathione; active stiffness; passive stiffness
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