Witowski Nancy E, Lusczek Elizabeth R, Determan Charles E, Lexcen Daniel R, Mulier Kristine E, Wolf Andrea, Ostrowski Beverly G, Beilman Greg J
Department of Surgery, University of Minnesota, Minneapolis, MN, USA.
Minnesota NMR Center, University of Minnesota, Minneapolis, MN, USA.
Mol Biosyst. 2016 Apr 26;12(5):1638-52. doi: 10.1039/c5mb00637f.
Hemorrhagic shock, a result of extensive blood loss, is a dominant factor in battlefield morbidity and mortality. Early rodent studies in hemorrhagic shock reported carbohydrate feeding prior to the induction of hemorrhagic shock decreased mortality. When repeated in our laboratory with a porcine model, carbohydrate pre-feed resulted in a 60% increase in death rate following hemorrhagic shock with trauma when compared to fasted animals (15/32 or 47% vs. 9/32 or 28%). In an attempt to explain the unexpected death rate for pre-fed animals, we further investigated the metabolic profiles of pre-fed non-survivors (n = 15) across 4 compartments (liver, muscle, serum, and urine) at specific time intervals (pre-shock, shock, and resuscitation) and compared them to pre-fed survivors (n = 17). As hypothesized, pre-fed pigs that died as a result of hemorrhage and trauma showed differences in their metabolic and physiologic profiles at all time intervals and in all compartments when compared to pre-fed survivors. Our data suggest that, although all animals were subjected to the same shock and trauma protocol, non-survivors exhibited altered carbohydrate processing as early as the pre-shock sampling point. This was evident in (for example) the higher levels of ATP and markers of greater anabolic activity in the muscle at the pre-shock time point. Based on the metabolic findings, we propose two mechanisms that connect pre-fed status to a higher death rate: (1) animals that die are more susceptible to opening of the mitochondrial permeability transition pore, a major factor in ischemia/reperfusion injury; and (2) loss of fasting-associated survival mechanisms in pre-fed animals.
失血性休克是大量失血的结果,是战场上发病和死亡的主要因素。早期关于失血性休克的啮齿动物研究报告称,在诱导失血性休克前给予碳水化合物喂养可降低死亡率。当我们实验室在猪模型中重复该实验时,与禁食动物相比,碳水化合物预喂养导致失血性休克合并创伤后的死亡率增加了60%(15/32或47% 对比 9/32或28%)。为了解释预喂养动物意外死亡率的原因,我们进一步研究了预喂养的非存活动物(n = 15)在特定时间间隔(休克前、休克和复苏)跨4个区室(肝脏、肌肉、血清和尿液)的代谢谱,并将其与预喂养的存活动物(n = 17)进行比较。正如所假设的,与预喂养的存活动物相比,因出血和创伤而死亡的预喂养猪在所有时间间隔和所有区室的代谢和生理特征均存在差异。我们的数据表明,尽管所有动物都接受了相同的休克和创伤方案,但非存活动物早在休克前采样点就表现出碳水化合物代谢改变。这在(例如)休克前时间点肌肉中较高水平的ATP和更高合成代谢活性标志物中很明显。基于代谢结果,我们提出了两种将预喂养状态与更高死亡率联系起来的机制:(1)死亡的动物更容易发生线粒体通透性转换孔开放,这是缺血/再灌注损伤的一个主要因素;(2)预喂养动物中与禁食相关的存活机制丧失。