Temporal changes in cardiac force- and flow-generation capacity, loading conditions, and mechanical efficiency in streptozotocin-induced diabetic rats.
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 (E(max)) and maximum theoretical flow (Q(max)) 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 E(max), Q(max) 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 Q(max), whereas ventriculoarterial uncoupling attenuated the cardiac mechanical efficiency in diabetic animals. The changes in E(max) and Q(max) are discordant during the progression of contractile dysfunction in the diabetic heart. In conclusion, our study showed that depressed Q(max) and cardiac mechanical efficiency, occurring preceding overt systolic heart failure, are two major determinants of deteriorating cardiac performance in diabetic rats.
Department of Cardiology, Far Eastern Memorial Hospital, Pan-Chiao, Taipei, Taiwan.
Dong-Feng
DF
Yeih
Lian-Yu
LY
Lin
Hung-I
HI
Yeh
Yu-Jun
YJ
Lai
Fu-Tien
FT
Chiang
Chuen-Den
CD
Tseng
Shu-Hsun
SH
Chu
Yung-Zu
YZ
Tseng
D000465:Algorithms; D000818:Animals; D001786:Blood Glucose / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology; D001835:Body Weight / Q000502:physiology; D002302:Cardiac Output / Q000502:physiology; D003921:Diabetes Mellitus, Experimental / Q000503:physiopathology*; D004548:Elasticity; D006321:Heart / Q000503:physiopathology*; D008297:Male; D009200:Myocardial Contraction / Q000502:physiology*; D009206:Myocardium / Q000201:enzymology; D052250:Nitric Oxide Synthase Type III / Q000096:biosynthesis; D051381:Rats; D017208:Rats, Wistar; D013318:Stroke Volume / Q000502:physiology; D014655:Vascular Resistance / Q000502:physiology; D016277:Ventricular Function, Left / Q000502:physiology
D001786:Blood Glucose; D052250:Nitric Oxide Synthase Type III