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1Department of Cardiology, Far Eastern Memorial Hospital, Pan-Chiao, Taipei; 3Departments of Internal Medicine and Medical Research, Mackay Memorial Hospital; Mackay Medicine, Nursing and Management College, Taipei Medical University, Taipei; 2Department of Internal Medicine, National Taiwan University Hospital, Taipei; and 4Department of Cardiology, Show Chwan Memorial Hospital, Chang-Hua, Taiwan
Submitted 17 May 2007 ; accepted in final form 24 November 2007
Diabetes mellitus may result in impaired cardiac contractility, but the underlying mechanisms remain unclear. We aimed to investigate the temporal alterations in cardiac force- and flow-generation capacity and loading conditions as well as mechanical efficiency in the evolution of systolic dysfunction in streptozotocin (STZ)-induced diabetic rats. Adult male Wistar rats were randomized into control and STZ-induced diabetic groups. Invasive hemodynamic studies were done at 8, 16, and 22 wk post-STZ injection. Maximal systolic elastance (Emax) and maximum theoretical flow (Qmax) were assessed by curve-fitting techniques, and ventriculoarterial coupling and mechanical efficiency were assessed by a single-beat estimation technique. In contrast to early occurring and persistently depressed Emax, Qmax progressively increased with time but was decreased at 22 wk post-STZ injection, which temporally correlated with the changes in cardiac output. The favorable loading conditions enhanced stroke volume and Qmax, whereas ventriculoarterial uncoupling attenuated the cardiac mechanical efficiency in diabetic animals. The changes in Emax and Qmax are discordant during the progression of contractile dysfunction in the diabetic heart. In conclusion, our study showed that depressed Qmax and cardiac mechanical efficiency, occurring preceding overt systolic heart failure, are two major determinants of deteriorating cardiac performance in diabetic rats.
diabetes; contractile function; hemodynamics; mechanical efficiency; ventriculoarterial coupling
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