Diabetes Mellitus
(DM) is a main risk factor for heart failure. A hallmark of this common
complication is a disturbed conductibility of the left ventricle (LV). In this
regard, diabetic cardiomyopathy is a significant entity, which could manifest
as impaired cardiac performance in the absence of coronary artery disease,
systemic hypertension or valvular heart disease that result from metabolic derangement
present in diabetes. Among others, structural changes in extracellular matrixand myocyte damage contain hallmarks of this disease. Abnormalities in these
compartments may result in left ventricular dysfunction (LV).
The Application
of streptozotozin (STZ) to rats is a well established model of type 1 DM. We
previously showed in this model severe impaired LV function under basal
conditions in a chronic stage of STZ-induced DM. We further identified
pathophysiological mechanisms, which could be responsible for this disturbed
cardiac phenotype. This includes endothelial dysfuntion, cardiac fibrosis,
inflammation and disturbed myocardial calcium regulation as well as
neurohumoral activation.Whereas the
cardiac phenotype under basal conditions in the chronic stage in STZ rats is
well characterized, we analysed in the present study in vivo the time-dependent
LV conductibility in this model. Therefore we measured LV function in STZ
diabetic rats on two different time points under basal and under different
pharmacological stress conditions using invasive LV microconductance catheter
technique. Read more................
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