Abstract： Objective To investigate the effects of calcium preconditioning (CP) on immature myocardial cell apoptosis and apoptosisregulated proteins. Methods The experiment was carried out from June 2000 to December 2001 in the Renmin Hospital of Wuhan University. Twelve rabbits with the age of 1421 d and the weight of 230300 g were divided into 2 groups with 6 in each group by random digital table. For rabbits in the ischemia/reperfusion group (I/R group), after Langendorff models were routinely set up, KrebsHenseleit (KH) solution was perfused for 20 minutes and reperfused for 120 minutes after 45 minutes of ischemia. For rabbits in the CP group, after Langendorff models were established, KH solution was perfused for20 minutes, and 45 seconds’ noncalcium KH solution perfusion and 5 minutes’ KH solution perfusion were repeated 3 times before 45 minutes of ischemia and 120 minutes of reperfusion of KH solution. In situ apoptosis identification and semiquantitative analysis were used to detect the myocardial cell apoptosis; agarose gel electrophoresis was used to detect the nucleosomal ladder of DNA fragments; and the expression of bcl-2, bax and fas were detected with Western blot method. Results The apoptosis rate for the CP group was lower than that of the I/R group (4.53%±1.22% vs. 12.30%±2.12%,t=7.780, P=0.000). Nucleosomal ladder of DNA fragments of the CP group was lower than that of the I/R group (OD value: 56 460±1 640 vs. 135 212±3 370,t=51.460,P=0.000). The expression of bcl-2 in the I/R group was lower than that of the CP group (OD value: 13 217±1 770 vs. 31 790±1 018,t=22.280, P=0.000). The expression of bax (OD value: 30 176±1 025 vs. 7 954±730, t=43.260, P=0.000) and fas (OD value: 29 197±1 233 vs. 8 140±867, t=34.220, P=0.000) in the I/R group was higher than that of the CP group. Conclusion CP can affect the expression of myocardial bcl-2, bax, and fas, and decrease immature myocardial cell apoptosis.
Objective To review the treatment methods and techniques of ischemia-reperfusion injury of flap. Methods Recent basic research l iterature concerning ischemia-reperfusion injury of flap was reviewed and analyzed in terms of treatment techniques. Results Ischemia-reperfusion injury is one of the leading causes of flap necrosis postoperatively. Interventions against any l ink of the ischemia-reperfusion injury progress could effectively reduce the damageand improve the survival rate of flaps. Conclusion Including production of reactive oxygen species, neutrophil infiltrationetc are thought to be the main mechanisms of ischemia-reperfusion injury. Treatment including medicine administration and physical intervention against any specific l ink of ischemia-reperfusion injury can interfere or block the whole progress, which reduce the damage of ischemia-reperfusion injury and improve the survival rate of animal flap models eventually.