Cardiac Sciences Program, University of Manitoba, St Boniface Hospital, Winnipeg, Manitoba, Canada.
J Heart Lung Transplant. 2013 Jul;32(7):734-43. doi: 10.1016/j.healun.2013.04.016.
Ex vivo heart perfusion (EVHP) has been proposed as a means to facilitate the resuscitation of donor hearts after cardiocirculatory death (DCD) and increase the donor pool. However, the current approach to clinical EVHP may exacerbate myocardial injury and impair function after transplant. Therefore, we sought to determine if a cardioprotective EVHP strategy that eliminates myocardial exposure to hypothermic hyperkalemia cardioplegia and minimizes cold ischemia could facilitate successful DCD heart transplantation.
Anesthetized pigs sustained a hypoxic cardiac arrest and a 15-minute warm ischemic standoff period. Strategy 1 hearts (S1, n = 9) underwent initial reperfusion with a cold hyperkalemic cardioplegia, normothermic EVHP, and transplantation after a cold hyperkalemic cardioplegic arrest (current EVHP strategy). Strategy 2 hearts (S2, n = 8) underwent initial reperfusion with a tepid adenosine-lidocaine cardioplegia, normothermic EVHP, and transplantation with continuous myocardial perfusion (cardioprotective EVHP strategy).
At completion of EVHP, S2 hearts exhibited less weight gain (9.7 ± 6.7 [S2] vs 21.2 ± 6.7 [S1] g/hour, p = 0.008) and less troponin-I release into the coronary sinus effluent (4.2 ± 1.3 [S2] vs 6.3 ± 1.5 [S1] ng/ml; p = 0.014). Mass spectrometry analysis of oxidized pleural in post-transplant myocardium revealed less oxidative stress in S2 hearts. At 30 minutes after wean from cardiopulmonary bypass, post-transplant systolic (pre-load recruitable stroke work: 33.5 ± 1.3 [S2] vs 19.7 ± 10.9 [S1], p = 0.043) and diastolic (isovolumic relaxation constant: 42.9 ± 6.7 [S2] vs 65.2 ± 21.1 [S1], p = 0.020) function were superior in S2 hearts.
In this experimental model of DCD, an EVHP strategy using initial reperfusion with a tepid adenosine-lidocaine cardioplegia and continuous myocardial perfusion minimizes myocardial injury and improves short-term post-transplant function compared with the current EVHP strategy using cold hyperkalemic cardioplegia before organ procurement and transplantation.
离体心脏灌注(EVHP)已被提议作为一种手段,以促进心肺死亡(DCD)后供体心脏的复苏,并增加供体池。然而,目前临床 EVHP 的方法可能会加重心肌损伤,并损害移植后的功能。因此,我们试图确定一种心脏保护的 EVHP 策略,该策略可以消除心肌对低温高钾停搏液的暴露,并最大限度地减少冷缺血,从而促进成功的 DCD 心脏移植。
麻醉猪经历缺氧性心脏骤停和 15 分钟的温缺血停搏期。策略 1 心脏(S1,n = 9)最初用冷高钾停搏液再灌注,进行体温 EVHP,并在冷高钾停搏液心脏骤停后进行移植(当前 EVHP 策略)。策略 2 心脏(S2,n = 8)最初用温热的腺苷-利多卡因停搏液再灌注,进行体温 EVHP,并进行连续心肌灌注(心脏保护 EVHP 策略)。
在 EVHP 完成时,S2 心脏的体重增加较少(9.7 ± 6.7[S2] vs 21.2 ± 6.7[S1]g/h,p = 0.008),冠状窦流出液中的肌钙蛋白-I 释放较少(4.2 ± 1.3[S2] vs 6.3 ± 1.5[S1]ng/ml;p = 0.014)。移植后心肌胸膜的质谱分析显示 S2 心脏的氧化应激较小。心肺旁路脱机后 30 分钟,移植后收缩功能(预负荷可募集的冲程工作:33.5 ± 1.3[S2] vs 19.7 ± 10.9[S1],p = 0.043)和舒张功能(等容松弛常数:42.9 ± 6.7[S2] vs 65.2 ± 21.1[S1],p = 0.020)在 S2 心脏中更好。
在 DCD 的这个实验模型中,与使用冷高钾停搏液进行器官获取和移植前的当前 EVHP 策略相比,使用温热的腺苷-利多卡因停搏液进行初始再灌注和连续心肌灌注的 EVHP 策略可最大程度地减少心肌损伤并改善移植后的短期功能。