Abstract
Diabetes mellitus is often associated with abnormalities in active relaxation and passive stiffness of the left ventricle but the molecular mechanisms responsible for the dysfunction are not yet clear. This study was designed to identify the molecular components that are responsible for the increased myocardial stiffness associated with diabetes. Multicelluar myocardial preparations were isolated from control Sprague-Dawley rats and an experimental group of rats injected 4 weeks previously with streptozotocin (model of Type I Diabetes). Preparations were subjected to paired ramp stretches/releases imposed under fiber length control in a series of calcium activations (pCa 4.5 - 9.0). The relative short-range force and elastic limits were substantially higher in the diabetic groups. The rate of tension recovery (ktr) was considerably lower in the diabetic groups. Short range stiffness values did not differ in the control and diabetic animals. Gel electrophoresis showed that the relative content of slower beta Myosin heavy chain increased from 34±15% in control hearts to 100% in the diabetic rat hearts. These results support the hypothesis that pathological changes in the mechanical properties of diabetic rat myocardium are mostly due to alterations in the active component (cycling cross-bridges) of ventricular stiffness.View Large Image | View Hi-Res Image | Download PowerPoint Slide
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