Figure 2

Depressed cardiac contractility in diabetic rats prevented by TETA-treatment. Depressed cardiac contractility in diabetic rats was prevented by TETA-treatment, which by contrast did not modify diabetes-induced alterations in [Ca²⁺]_i homeostasis. (A) Diabetic rats showed unchanged peak (i) and resting (ii) [Ca²⁺]_i values but had concomitantly decreased peak stress (iii) (Diabetic: 10 ± 1 mN/mm²; Control: 17 ± 2 mN/mm², P = 0.02) and unchanged resting stress (iv). TETA-treatment preserved peak stress in diabetic rats (TETA-treated diabetic: 20 ± 4 mN/mm², P = 0.04) but did not significantly modify peak or resting [Ca²⁺]_i. (B) The time course of the Ca²⁺ transient was prolonged in diabetic rats: (time-to-peak [Ca²⁺]_i (i); and time constant of decay of the Ca²⁺ transient (ii)), as was the time course of isometric stress (time-to-peak stress (iii); and time-to-90% relaxation (iv)). However, TETA-treatment had no effect on the time course of either variable. (C) The maximum rate of rise in the Ca²⁺ transient was unchanged (i) whereas the maximum rate of stress development was decreased in diabetic rats (ii), and this decrease was prevented by TETA-treatment. C: Control (Open bars, n = 10); D: Diabetic (Solid bars, n = 8); D + T: TETA-treated diabetic (Patterned bars, n = 7). Data are means ± SEM, one-way ANOVA with application of the post-hoc Holm-Sidak test: * C vs D; ‡ C vs D + T; † D vs D + T; P < 0.05.