超速起搏预适应的延迟保护作用与血红素氧合酶-1的关系

目的：探讨超速心室起搏（VOP）预适应的延迟保护作用与心肌血红素氧合酶-1（HO—1）表达的关系。方法：健康的新西兰兔24只，按数字表法随机均分为（1）：对照组（单纯结扎组）：将电极送至右心室旷置70min;（2）起搏组：以500次／min起搏右心室10min×4次；（3）起搏＋放线菌素D组：予静脉注射放线菌素D0．1mg／kg后按起搏组方法起搏右心室。24h后所有实验动物开胸结扎冠脉前降支造成缺血再灌注模型，缺血再灌注前后检测肌酸激酶（CK）和肌酸激酶同工酶（CK—MB），动态描记再灌注时心电图；免疫组织化染色检测心肌组织H0—1表达。结果：（1）缺血再灌注后，与单纯结扎组比较，起搏组在再灌注不同时相CK[60min：（3723±735）IU／L比（2163±602）IU／L]和CK—MB[60min：（1709±163）IU／L比（904±149）IU／L]水平均显著降低（P〈0.01）；起搏＋放线菌素D组介于起搏组与单纯结扎组之间（P〈0.01）；（2）单纯结扎组在再灌注过程中共有5只、62．5％）发生心律失常，起搏＋放线菌素D组有4只（50％），而起搏组无心律失常发生。起搏组心律失常发生率显著低于单纯结扎组（0比62．5％，P〈0.05）；（3）起搏组HO-1的阳性表达的程度明显高于单纯结扎组和起搏＋放线菌素D组（P〈0.05，〈0．01）。结论：超速起搏预适应可以模拟缺血预适应，产生延迟保护作用，减少心肌组织的坏死和心律失常的发生，并伴有血红素氧合酶-1表达增加，其作用可能与心肌组织血红素氧合酶-1的表达增加有关。

Relationship between delayed protection of overdrive pacing preconditioning and heme oxygenase - 1

Objective.. To explore the relationship between delayed protection of ventricular overdrive pacing （VOP） preconditioning and expression of myocardial heme oxygenase- 1 （HO- 1）. Methods.. A total of 24 healthy New Zealand rabbits were randomly and equally divided into control group （pure ligation group, electrode was sent to right ventricle and placed for 70min）, pacing group （right ventricle was paced at 500 times/min, 10min × four times） and pacing ± actinomycin D group （0. 1mg/kg actinomycin D was injected intravenously before right ventricle was paced as pacing group） according to number table. After 24h, ischemia/reperfusion （I/R） model was established in all rabbits via thoracotomy and ligation of coronary anterior descending branch. Levels of creatine kinase （CK） and CK isoenzyme （CK - MB） were measured before and after I/R; electrocardiogram was dynamically recorded during reperfusion; immunohistochemistry staining was used to measure expression of HO- 1 in myocardial tissues. Results： （1） Compared with pure ligation group after I/R, there were significant decrease in levels of CK [60min： （3723 ± 735） IU/L vs. （2163 ± 602） IU/L] and CK - MB [60min.. （1709 ± 163） IU/L vs. （904 ± 149） IU/ L] in pacing group at different time phase of reperfusion, P〉0.01; those of pacing ＋ actinomycin D group were between pacing group and pure ligation group, P〈0.01; （2） During reperfusion, there were five rabbits （62.5%）, four rabbits （50%） and no rabbit occurring arrhythmias in pure ligation group, pacing ＋ actinomycin D group and pacing group respectively. Compared with pure ligation group, there was significant decrease in incidence rate of arrhythmia （62.5% vs. 0, P〈0.05） in pacing group; （3） Positive expression level of HO- 1 in pacing group was significantly higher than those of pure ligation group （ P〈0. 05） and pacing ＋ actinomycin D group （P〈0.01）. Conclusion： Overdrive pacing preconditioning can mimic ischemic preconditioning, produce delayed protection, decrease myocardial tissue necrosis and arrhythmia, significantly increase HO- 1 expression; its protection may be related to increased expression of HO- 1.