Objectives To explore the effect of cyclovirobuxin-D(CVB-D) on intracellular calcium in electrically stimulated ventricular myocytes of diabetic rats
Methods Diabetes was induced in male SD rats, using a single injection of alloxan into tail vein. untreated age-matched animals were used as controls. The ventricular myocytes were isolated with collagenase (type 1) and the spectrofluorometric method was used to measure the intracellular calcium. Fura-2/AM was used as calcium fluorescence probe.
Results There was no different of end-diastolic calcium and electrically stimulated intracellular calcium transient as well as peak transient between 6th week diabetic rats and control (P > 0.05). CVB-D (0.1∼1 μmol·L-1 ) showed no significantly action on electrically stimulated intracellular calcium transient both of 6th week diabetic rats and control. However, CVB-D (2∼5 μmol·L-1) increased the electrically stimulated intracellular calcium transient amplitude from control rats (P < 0.05), Whilst significantly decreased electrically stimulated intracellular calcium transient amplitude from 6th week diabetic rats (P < 0.01). CVB-D (0.1∼5 μmol·L-1 ) showed no significantly action onend-diastolic calcium level from diabetic and control rats. Additionally, CVB-D 2 μmol·L-1 , at perfusing 15min, appeared potentiation on the electrically stimulated intracellular calcium transient from control ratsand attenuation on that of diabetes. Finally, there appeared significant prolongation of time to peak and time to relaxation of calcium transient from diabetic rats (P < 0.01). CVB-D prolongated time to peak from diabetic rats and control, but there was no difference between the two groups. While CVB-D showed no significant action on the time to relaxation of diabetic rats and control.
Conclusions The prolongation of calcium transient time probably was responsive for decline of diabetic heart function. CVB-D the amplitude of calcium transient and prolongated the time to peak of calcium transient from diabetic rats, that was probably associated with CVB-D-depressing myocardium contractile function from 6th week diabetic rats.