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1 Department of Cardiology, Far Eastern Memorial Hospital, Taipei, Taiwan - Republic of China; Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan - Republic of China
2 Department of Internal Medicine, National Taiwan University Hospital, Taipei, Taiwan - Republic of China
3 Departments of Internal Medicine and Medical Research, Mackay Memorial Hospital, Taipei, Taiwan - Republic of China
4 Department of Cardiology, Far Eastern Memorial Hospital, Taipei, Taiwan - Republic of China
5 Department of Internal Medicine, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan - Republic of China; Department of Cardiology, Show Chwan Memorial Hospital, Chang-Hua, Taiwan - Republic of China
* To whom correspondence should be addressed. E-mail: yztseng{at}ntu.edu.tw.
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 weeks post STZ injection. Maximal systolic elastance (Emax) and maximum theoretical flow (Qmax) were assessed by curve fitting techniques; ventriculoarterial coupling and mechanical efficiency 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 wks post STZ injection, which temporally correlated with the changes in cardiac output. The favorable loading conditions enhanced stroke volume and Qmax, while 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.
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