alexa Reduced Cardiac Performance after Differential Pharmacological Stress in Streptozotocin-Induced Diabetic Rats
ISSN: 2155-9880

Journal of Clinical & Experimental Cardiology
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Research Article

Reduced Cardiac Performance after Differential Pharmacological Stress in Streptozotocin-Induced Diabetic Rats

Alexander Riad1*, Dirk Westermann2, Stephan B Felix1, Heinz P Schultheiss2 and Carsten Tschope2
1Ernst-Moritz-Arndt-Universität, Klinik für Innere Medizin B, Friedrich-Löffler-Strasse 23A, 17475 Greifswald, Germany
2Charite – Universitätsmedizin Berlin, Campus Benjamin Franklin, Department of Cardiology and Pulmology Hindenburgdamm 30, 12203 Berlin, Germany
Corresponding Author : Dr. med. Alexander Riad
Facharzt für Innere Medizin
Universitätsklinik der Ernst-Moritz-Arndt-Universität
Innere Klinik B, Friedrich-Löffler-Strasse 23 a, 17475 Greifswald
Tel: 03834-86-5658
Fax: 03834-86-6657
E-mail: [email protected]
Received October 25, 2010; Accepted November 02, 2010; Published November 04, 2010
Citation: Riad A, Westermann D, Felix SB, Schultheiss HP, Tschope C (2010) Reduced Cardiac Performance after Differential Pharmacological Stress in Streptozotocin-Induced Diabetic Rats. J Clinic Experiment Cardiol 1:108. doi:10.4172/2155-9880.1000108
Copyright: © 2010 Riad A, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
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Abstract

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 fi ndings, the maximum LV conductibility induced by adrenalin was signifi cantly 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.

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