Ludwig Boltzmann Institute for Experimental and Clinical Traumatology, AUVA Research Center for Traumatology, 1200 Vienna, Austria.
Thermo Fisher Scientific, BRAHMS Biomarkers, Research Department, 16761 Hennigsdorf, Germany.
Molecules. 2018 Aug 30;23(9):2195. doi: 10.3390/molecules23092195.
Background aim: Reperfusion after hemorrhagic traumatic shock (HTS) is often associated with complications that are partly ascribed to the formation of reactive oxygen species (ROS). The aim of our study was to compare the effects of restrictive reperfusion (RR) to rapid full reperfusion (FR) on ROS formation and/or oxidative events.
Anesthetized male rats were randomly subjected to HTS followed by FR (75 mL/kg/h) or RR (30 mL/kg/h for 40 min, followed by 75 mL/kg/h) with Ringer's solution (n = 8/group). Compartment-specific ROS formation was determined by infusion of ROS scavenger 1-hydroxy-3-carboxy-2,2,5,5-tetramethyl-pyrrolidine hydrochloride (CP-H) during resuscitation, followed by electron paramagnetic resonance spectroscopy. Sham-operated animals (n = 8) served as controls. The experiment was terminated 100 min post-shock.
Mean arterial pressure was significantly higher in the FR compared to the RR group during early reperfusion. Only RR animals, not FR animals, showed significantly higher ROS concentrations in erythrocytes (1951 ± 420 vs. 724 ± 75 AU) and in liver (474 ± 57 vs. 261 ± 21 AU) compared to sham controls. This was accompanied by elevated alanine aminotransferase and creatinine levels in RR animals compared to both shams and FR animals, while lipid peroxidation products (thiobarbituric acid reactive substances) were significantly increased only in the kidney in the FR group ( < 0.05). RR animals showed significantly higher plasma peroxiredoxin-4 values when compared to the FR group (20 ± 2 vs. 14 ± 0.5 RLU).
Restrictive reperfusion after HTS is associated with increased ROS formation in erythrocytes and liver compared to sham controls. Moreover, the restrictive reperfusion is associated with a more pronounced injury to the liver and kidney, which is likely mediated by other than lipid peroxidation process and/or oxidative stress reactions.
出血性创伤性休克（HTS）后的再灌注常伴有并发症，部分归因于活性氧（ROS）的形成。我们的研究旨在比较限制再灌注（RR）与快速完全再灌注（FR）对 ROS 形成和/或氧化事件的影响。
麻醉雄性大鼠随机接受 HTS 后接受 FR（75 mL/kg/h）或 RR（30 mL/kg/h 40 min，然后 75 mL/kg/h）用林格氏液（n = 8/组）。复苏过程中通过输注 ROS 清除剂 1-羟基-3-羧基-2,2,5,5-四甲基吡咯烷盐酸盐（CP-H）来确定特定隔室的 ROS 形成，然后进行电子顺磁共振光谱。假手术动物（n = 8）作为对照。实验在休克后 100 分钟终止。
FR 组再灌注早期的平均动脉压明显高于 RR 组。只有 RR 组动物，而不是 FR 组动物，红细胞（1951 ± 420 比 724 ± 75 AU）和肝脏（474 ± 57 比 261 ± 21 AU）中的 ROS 浓度明显高于假对照。与 sham 和 FR 动物相比，RR 动物的丙氨酸氨基转移酶和肌酐水平升高，而只有 FR 组的肾脏中的脂质过氧化产物（硫代巴比妥酸反应物质）显著增加（<0.05）。与 FR 组相比，RR 组动物的血浆过氧化物酶-4 值明显升高（20 ± 2 比 14 ± 0.5 RLU）。
与 sham 对照组相比，HTS 后限制再灌注与红细胞和肝脏中 ROS 形成增加有关。此外，限制再灌注与肝脏和肾脏的损伤更明显有关，这可能是由脂质过氧化过程和/或氧化应激反应以外的机制介导的。
