In recent years, it was found that heart was significantly protected against ischemia-reperfusion injury if it was first preconditioned by brief ischemia or by administering a potassium channel opener. Both of these preconditioning strategies were found to require opening of a K(ATP) channel, we showed that this pivotal role was mediated by the mitochondrial ATP-sensitive K+ channel (mitoK(ATP)). As the mechanism was not clarified yet, this paper reviewed the evidence showing that the mechanism and the characters of mito K(ATP) and its cardioprotection against ischemia-reperfusion injury

Objective To evaluate the effects of hydrogen peroxide (H 2O 2) on cardiomyocytes and the protective effect of pinacidil preconditioning on injured primary cultured cardiomyocytes. Methods We isolated and cultured cardiomyocytes in neonatal mice by trypsin digestion technique. The cells were inoculated in 96-well culture plate at the density of 1?10 5/ml. Cells were divided into control group and 400, 600, and 800 ?mol/L H 2O 2 treatment groups. MTT assay was used to determine the cell vitality at 1, 3, 6, 12, and 24 h after H 2O 2 treatment. The effects of pinacidil preconditioning were also observed. Results The effect of H 2O 2 on the damages to cardiomyocytes was in dose- and time-dependent manners. Pretreatment with pinacidil at the concentrations of 1?10 -4 , 1?10 -5 , and 1?10 -6 mol/L, particularly 1?10 -6 mol/L, could increase the activity of cardiomyocytes treated with H 2O 2. Conclusion Pinacidil preconditioning at lower doses can protected cardiomyocytes from injuries induced by H 2O 2.

Objective To investigate the protective effect of pinacidil on the intestinal mucosa of scalded rats and the mechanism. Methods A total of 24 healthy SD rats were randomly divided into normal control group, burn group, and pinacidil treated group. Rats in burn group and pinacidil treated group were inflicted with 30% TBSA Ⅲ degree burn and resuscitated intraperitoneally with Ringer's solution immediately after burn. Pinacidil was injected intraperitoneally into rats in pinacidil treated group at the dose of 2 mg/kg. Mitochondrial respiratory function intestinal mucosa and levels of reactive oxygen species (ROS), maleic dialdehyde (MDA), and superoxide dismutase (SOD) in plasma were determined at 6 h after burn. Results Mitochondrial respiratory function control rate (RCR), ST3, and SOD levels in pinacidil treated group were evidently higher than those in the burn group. However, ST4, MDA, and ROS levels in pinacidil treated group were significantly lower than those in the burn group, but ST4 was not significantly different from that in the normal control. Conclusion Pinacidil can attenuate the damage of intestinal mucosa in scalded rats.