1. In order to clarify whether the myocardial dysfunction observed in diabetic-rat hearts is an intrinsic property of the myocytes or not, we investigated cardiac function and myocyte contractile function in diabetic rats 5 weeks after the injection of streptozotocin.

2. Maximal and minimal dP/dt and time constant of isovolumic pressure fall were measured using a micromanometer in diabetic and age-matched control rats.

3. Isolated myocytes were enzymically obtained from each rat heart and were stimulated at 1 Hz (37°C) in a buffer containing 1.5 mmol/l Ca2+. The images of myocyte contractions were recorded by a video system. Normalized maximal velocity of shortening (maximal velocity of cell shortening/resting cell length; s−1), normalized maximal velocity of relengthening (maximal velocity of cell relengthening/resting cell length; s−1) and extent of shortening [(twitch amplitude/resting cell length) × 100;%] were analysed by a digitalized computer as contractile functions of the myocyte.

4. The maximal and minimal dP/dt in diabetic rats (7876, 5341 mmHg/s) were significantly lower than those in control rats (9349, 7876 mmHg/s). The time constant of isovolumic pressure fall in diabetic rats (12.7 ms) was significantly greater than that in control rats (8.6 ms). Moreover, the normalized maximal velocity of shortening, normalized maximal velocity of relengthening and extent of shortening in myocytes from diabetic rats (1.40 s−1, 1.38 s−1, 9.5%) were significantly lower than those in myocytes from control rats (1.64 s−1, 1.60 s−1, 11.8%).

5. These results suggest that contractile impairment in this diabetic-rat heart model is mainly due to an intrinsic abnormality of the cardiac myocytes.

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