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Research Article Free access | 10.1172/JCI114734

Abnormal cardiac function in the streptozotocin-diabetic rat. Changes in active and passive properties of the left ventricle.

S E Litwin, T E Raya, P G Anderson, S Daugherty, and S Goldman

Department of Internal Medicine, Veterans Administration Medical Center, Tucson, Arizona 85723.

Find articles by Litwin, S. in: PubMed | Google Scholar

Department of Internal Medicine, Veterans Administration Medical Center, Tucson, Arizona 85723.

Find articles by Raya, T. in: PubMed | Google Scholar

Department of Internal Medicine, Veterans Administration Medical Center, Tucson, Arizona 85723.

Find articles by Anderson, P. in: PubMed | Google Scholar

Department of Internal Medicine, Veterans Administration Medical Center, Tucson, Arizona 85723.

Find articles by Daugherty, S. in: PubMed | Google Scholar

Department of Internal Medicine, Veterans Administration Medical Center, Tucson, Arizona 85723.

Find articles by Goldman, S. in: PubMed | Google Scholar

Published August 1, 1990 - More info

Published in Volume 86, Issue 2 on August 1, 1990
J Clin Invest. 1990;86(2):481–488. https://doi.org/10.1172/JCI114734.
© 1990 The American Society for Clinical Investigation
Published August 1, 1990 - Version history
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Abstract

To provide an integrated assessment of changes in systolic and diastolic function in diabetic rats, we measured conscious hemodynamics and performed ex vivo analysis of left ventricular passive-elastic properties. Rats given streptozotocin (STZ) 65 mg/kg i.v. (n = 14) were compared with untreated age-matched controls (n = 15) and rats treated with insulin after administration of STZ (n = 11). After 7 d, diabetic rats exhibited decreases in heart rate and peak developed left ventricular (LV) pressure during aortic occlusion. After 26 d of diabetes there were significant decreases in resting LV systolic pressure, developed pressure, and maximal +dP/dt, whereas LV end-diastolic pressure increased and the time constant of LV relaxation was prolonged. The passive LV pressure-volume relationship was progressively shifted away from the pressure axis, and the overall chamber stiffness constant was decreased. However, "operating chamber stiffness" calculated at end-diastolic pressure was increased at 7 d, and unchanged at 26 d. LV cavity/wall volume and end-diastolic volume were increased after 26 d of diabetes. Myocardial stiffness was unchanged at both time intervals. All of the above abnormalities were reversed by the administration of insulin. We conclude that the hemodynamic and passive-elastic changes that occur in diabetic rats represent an early dilated cardiomyopathy which is reversible with insulin.

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