*Department of Anesthesiology, University Hospital Ulm, Ulm, Germany †Institute of Anesthesiological Pathophysiology and Process Engineering, University Hospital Ulm, Ulm, Germany ‡Institute for Pathology, University Hospital Ulm, Ulm, Germany §Department X Anesthesia and Intensive Care Medicine, Bundeswehr Hospital Ulm, Ulm, Germany ||Department of Internal Medicine I, Biomedical Centre and Karlova Univerzita Praha, Plzeň, Czech Republic ¶CNRS UMR 6214, INSERM U1083, Université Angers, Angers, France **Département de Réanimation Médicale et de Médecine Hyperbare, Centre Hospitalier Universitaire, Angers, France.
Shock. 2017 Nov;48(5):564-570. doi: 10.1097/SHK.0000000000000884.
We previously demonstrated beneficial effects of 22 h of hyperoxia following near-lethal porcine hemorrhagic shock, whereas therapeutic hypothermia was detrimental. Therefore, we investigated whether shorter exposure to hyperoxia (12 h) would still improve organ function, and whether 12 h of hypothermia with subsequent rewarming could avoid deleterious effects after less severe hemorrhagic shock.Twenty-seven anesthetized and surgically instrumented pigs underwent 3 h of hemorrhagic shock by removal of 30% of the blood volume and titration of the mean arterial blood pressure (MAP) to 40 mm Hg. Post-shock, pigs were randomly assigned to control, hyperoxia (FIO2 100% for 12 h) or hypothermia group (34°C core temperature for 12 h with subsequent rewarming). Before, at the end of shock, after 12 and 23 h of resuscitation, data sets comprising hemodynamics, blood gases, and parameters of inflammation and organ function were acquired. Postmortem, kidney samples were collected for immunohistochemistry and western blotting.Hyperoxia exerted neither beneficial nor detrimental effects. In contrast, mortality in the hypothermia group was significantly higher compared with controls (67% vs. 11%). Hypothermia impaired circulation (MAP 64 (57;89) mm Hg vs. 104 (98; 114) mm Hg) resulting in metabolic acidosis (lactate 11.0 (6.6;13.6) mmol L vs. 1.0 (0.8;1.5) mmol L) and reduced creatinine clearance (26 (9;61) mL min vs. 77 (52;80) mL min) compared to the control group after 12 h of resuscitation. Impaired kidney function coincided with increased renal 3-nitrotyrosine formation and extravascular albumin accumulation.In conclusion, hyperoxia proved to be safe during resuscitation from hemorrhagic shock. The lacking organ-protective effects of hyperoxia compared to resuscitation from near-lethal hemorrhage suggest a dependence of the effectiveness of hyperoxia from shock severity. In line with our previous report, therapeutic hypothermia (and rewarming) was confirmed to be detrimental most likely due to vascular barrier dysfunction.
我们之前的研究表明，在接近致死性猪出血性休克后，22 小时的高氧暴露有益，而治疗性低温则有害。因此，我们研究了较短时间的高氧暴露（12 小时）是否仍能改善器官功能，以及在较轻程度的出血性休克后，12 小时的低温与随后的复温是否可以避免有害影响。27 头麻醉和手术仪器猪通过去除 30%的血液量并将平均动脉血压（MAP）滴定至 40mmHg 经历 3 小时的出血性休克。休克后，猪被随机分配到对照组、高氧组（12 小时 FIO2 为 100%）或低温组（34°C 核心体温 12 小时，随后复温）。在休克前、休克结束时、复苏后 12 小时和 23 小时，采集包括血流动力学、血气以及炎症和器官功能参数的数据组。死后，收集肾脏样本进行免疫组织化学和蛋白质印迹分析。高氧既没有有益也没有有害作用。相比之下，低温组的死亡率明显高于对照组（67%比 11%）。低温会损害循环（MAP 为 64（57；89）mmHg 比 104（98；114）mmHg），导致代谢性酸中毒（乳酸 11.0（6.6；13.6）mmol/L 比 1.0（0.8；1.5）mmol/L）和肌酐清除率降低（26（9；61）mL min 比 77（52；80）mL min）与复苏 12 小时后的对照组相比。肾功能受损与肾脏 3-硝基酪氨酸形成增加和血管外白蛋白积聚有关。总之，高氧在从出血性休克复苏过程中被证明是安全的。与从接近致死性出血性休克复苏相比，高氧没有器官保护作用，这表明高氧的有效性取决于休克的严重程度。与我们之前的报告一致，治疗性低温（和复温）被证实是有害的，很可能是由于血管屏障功能障碍。
