Hypoxic reoxygenation during initial reperfusion attenuates cardiac dysfunction and limits ischemia-reperfusion injury after cardioplegic arrest in a porcine model

Hypoxic reoxygenation during initial reperfusion attenuates cardiac dysfunction and limits ischemia-reperfusion injury after cardioplegic arrest in a porcine model
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DOI:
10.1016/j.jtcvs.2008.09.025
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发表时间:
2009-04-01
影响因子:
6
通讯作者:
Moritz, A.
Moritz, A.
中科院分区:
医学1区
文献类型:
--
作者:
Abdel-Rahman, U.;Risteski, P.;Moritz, A.

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目的:在临床实践中,缺血心肌再灌注常发生在高动脉血氧水平下。然而,这可能加重氧化应激过度引起的心脏缺血再灌注损伤。在一项体内实验研究中,评估了初始再灌注时缺氧再氧的心脏保护作用。方法:对21头成年猪进行主动脉交叉夹闭体外循环(90分钟)和心脏骤停。在初始再灌注时,10头猪进行了标准的缺氧再氧(PaO2, 250-350 mm Hg),而11头猪进行了逐渐的再氧(PaO2, 40-90 mm Hg)。采用热稀释法和导尿管技术分析心功能。结果:两组患者体外循环术后10分钟心脏指数均较术前下降。体外循环后60分钟,逐渐复氧后心脏指数较低氧复氧后明显改善(3.2 +/- 0.6 vs 2.5 +/- 0.5 L)。分钟(1)。m(-2), P = .04)。相应的,渐进式复氧组收缩期末压力-容积关系和左室压力峰值升高幅度明显小于渐进式复氧组。再灌注期间和再灌注后,逐渐复氧后冠状窦内丙二醛和肌钙蛋白T值均显著降低(去断路后60分钟:丙二醛,7.6 +/- 0.8 vs 4.6 +/- 0.5 μ mol/L [P = .007];肌钙蛋白,0.12 +/- 0.02 vs 0.41 +/- 0.12 ng/mL [P = .02])。结论:猪心肌缺血再灌注时缺氧复氧可减轻心肌缺血再灌注损伤,并有助于维持心肌缺血后的心脏功能。
Objective: In clinical practice, reperfusion of ischemic myocardium usually occurs under high arterial oxygen levels. However, this might aggravate cardiac ischemia-reperfusion injury caused by excessive oxidative stress. In an experimental in vivo study, the cardioprotective role of hypoxic reoxygenation during initial reperfusion was assessed.Methods: Twenty-one adult pigs were started on cardiopulmonary bypass with aortic crossclamping ( 90 minutes) and cardioplegic arrest. During initial reperfusion, 10 pigs underwent standard hypoxic reoxygenation (PaO2, 250-350 mm Hg), whereas gradual reoxygenation (PaO2, 40-90 mm Hg) was performed in 11 pigs. Cardiac function was analyzed by means of the thermodilution method and conductance catheter technique.Results: In both groups cardiac index was decreased 10 minutes after cardiopulmonary bypass compared with preoperative values. Sixty minutes after cardiopulmonary bypass, cardiac index improved significantly after gradual reoxygenation compared with that after hypoxic reoxygenation (3.2 +/- 0.6 vs 2.5 +/- 0.5 L . min(-1) . m(-2), P = .04). Correspondingly, end-systolic pressure-volume relationship and peak left ventricular pressure increase were significantly less decreased in the gradual reoxygenation group. During and after reperfusion, malondialdehyde and troponin T values within the coronary sinus were significantly lower after gradual reoxygenation ( 60 minutes after declamping: malondialdehyde, 7.6 +/- 0.8 vs 4.6 +/- 0.5 mu mol/L [P = .007]; troponin, 0.12 +/- 0.02 vs 0.41 +/- 0.12 ng/mL [P = .02]).Conclusion: Hypoxic reoxygenation at the onset of reperfusion attenuates myocardial ischemia-reperfusion injury and helps to preserve cardiac performance after myocardial ischemia in a pig model.