The development of heart failure including disturbed cardiac stress response is a main complication of diabetes mellitus (DM). In the present study we characterized in vivo the cardiac stress response in the often used streptozotocin (STZ) rat model. We analysed left ventricular (LV) performance of STZ-diabetic rats under basal and pharmacological stress conditions by recording pressure-volume loops using a microconductance catheter at two different time points.

Under basal conditions, STZ induces after two weeks impaired LV systolic and diastolic dysfunction indexed by decreased LV pressure and dp/dtmax as well as decreased cardiac stiffness and dp/dtmin leading to decreased cardiac output. This cardiac phenotype behaved at least in part progressively up to six weeks after STZ injection. Intravenously infusion of dobutamine led to a dose-dependent depression of LV performance two and six weeks after STZ injection. Concordant with these findings, the maximum LV conductibility induced by adrenalin was significantly decreased at both two and six weeks after STZ injection. The STZ-diabetic rat is an adequate model for investigating disturbed cardiac stress response as a result of diabetic conditions.

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 matrix and 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 neuro humoral 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.

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ISSN: 2155-9880

Current Issue: Volume 11, Issue 8

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