Objective: To investigate the effect of diazoxide (DE) on the myocardial ultrastructure and opening of maitochondrial permeability transition pore (MPTP) in donor rat heart suffered from long-term hypothermic preservation.
Methods: The Langendorff model of isolated rat heart was used. The hearts were stored in 4 degrees C Celsior solution containing different concentration of DE (15, 30, or 45 micromol/L) for 9 h followed by 60 min of reperfusion. The recovery of rate-pressure product (RPP) was observed. The opening of MPTP and myocardial mitochondria ultrastructure were also evaluated.
Results: (1) As compared with the celsior solution preserved group, DE (30 micromol/L) increased recovery of RPP during reperfusion and inhibited the opening of MPTP. DE also alleviated the myocardial mitochondrial ultrastucture damage induced by long-term hypothermic preservation. (2) The above effects of DE were attenuated by a mitoK(ATP) channel inhibitor 5-hydroxydecanoate and a MPTP opener atractyloside.
Conclusion: In the donor rat heart, DE protects myocardial mitochondria ultrastructure against long-term hypothermic preservation injury via inhibiting the opening of MPIP.