Objective   To investigate the effect of ischemic preconditioning (IP) on insulin sensitivity after cardiomyocyte calcium overload.    Methods   Adult rat cardiac myocytes were obtained through Langendorff perfusion with retrograde aortic infusion and collagenase digestion. Myocardial cells were divided into 5 groups

normal control group

experimental group 1 (ionomycin 0.5 μmol/L)

experimental group 2 (ionomycin 0.5 μmol/L+IP)

experimental group 3 (ionomycin 1.0 μmol/L)

the experimental group 4 (ionomycin 1.0 μmol/L+IP). The glucose uptake of cardiomyoctyes stimulated by insulin was detected with isotopic tracer technique.    Results   Rate of cardiac cell activity in each group had no significant decrease (P0.05). Resting [Ca

2+

]

i in normal cardiac muscle cells was (117±22.41) nmol/L

while for the cells of experimental groups 1 and 2

it was significantly higher than normal cells

but there was no significant difference between them after 1 hour’s treatment of 0.5 μmol/L ionomycin [(260.00±33.06) and (278±23.46) nmol/L respectively

]

. The [Ca

2+

]

i in experimental groups 3 and 4 was (391.00±20.01)

and (379.00±23.92) nmol/L respectively

which were significantly higher than those of experimental groups 1 and 2

and control group (P0.05). But there was no obvious difference between them. Insulin of 20 IU/L promoted glucose uptaking in the myocardial cells in each group

which were (56.86±6.89)

(31.10±7.62)

(40.12±6.90)

(22.26±5.92)

and (32.33±6.06) μmol/(10

5

cells·10 min) respectively in control

and experimental groups 1

2

3 and 4. There were significantly lesser glucose uptake in the insulin-stimulated myocardial cells from all experimental groups than in the cells of the control group (P0.05). Insulin-stimulated myocardial cells in experimental groups 2 and 4 though had lower glucose uptake than the control group

but their glucose uptake were higher in comparison with non-ischemic preconditioning group (P0.05). 

   Conclusion   IP has no effect on ionomycin-induced calcium overload in myocardial cells

but can improve myocardial insulin resistance after calcium overload.