Learning and memory is preserved after induced asanguineous hyperkalemic hypothermic arrest in a swine model of traumatic exsanguination
Learning and memory is preserved after induced asanguineous hyperkalemic hypothermic arrest in a swine model of traumatic exsanguination
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DOI：
10.1067/msy.2002.125787
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发表时间：
2002-08-01
期刊：
影响因子：
3.8
通讯作者：
Rhee, P
中科院分区：
文献类型：
--
作者：
Alam, HB;Bowyer, MW;Rhee, P
背景如果在创伤患者中安全诱导，诱导的无血低温代谢停止（假死）可以为修复主要血管损伤提供宝贵的时间。我们报告了一种新的方法，这样做的猪模型的不受控制的致死性出血（ULH），导致保存的学习能力和记忆。约克郡猪（100 - 125磅）在通过左胸廓切开术快速主动脉内输注低温（4 ℃）、高钾（70 mEq/L）器官保存液之前进行ULH。持续冷却，直到核心温度达到10 ℃，并使用低流量心肺转流维持60分钟。在假死状态下修复血管损伤，然后逆转假死状态，观察动物6周。通过训练动物从颜色编码的盒子中取出食物来测试认知功能。术后，记忆这项任务的能力和75分客观神经功能量表被用来测试神经功能。实验Ⅰ中，ULH由胸主动脉撕裂引起（n = 9）。5只术前未经训练的动物接受训练以执行任务，并与对照动物（n = 15）进行比较，4只术前经过训练的动物接受术后记忆保留测试。在实验II中，通过造成髂动脉和静脉损伤来诱导ULH（n = 15）。在诱导低氧血症之前，动物保持休克15、30和60分钟。在实验一中，存活的动物（719只）神经系统完好无损，它们学习新技能的能力与对照组动物没有什么不同。所有预先训练的动物均表现出完全的记忆保留。在实验II中，休克15、30和60分钟的存活率分别为80%、60%和80%。60分钟组中的所有动物（1只除外）神经系统完整，并显示出正常的学习能力。诱导低温代谢停止（通过开胸术）修复复杂创伤性损伤是可行的，即使在腹腔内来源的不受控制的出血引起的长时间休克后，也能保留正常的神经功能。
Background. Induced asanguineous hypothermic metabolic arrest (suspended animation) could provide valuable time to repair major vascular injuries if safely induced in patients with trauma. We report a novel method of doing this in a swine model of uncontrolled lethal hemorrhage (ULH) that resulted in preservation of learning ability and memory.Methods. Yorkshire swine (100 to 125 lb) underwent ULH before rapid intra-aortic infusion of a hypothermic (4degreesC), hyperkalemic (70 mEq/L) organ preservation solution by a left thoracotomy. Cooling continued until core temperature reached 10degreesC, and this was maintained for 60 minutes using low-flow cardiopulmonary bypass. Vascular injuries were repaired during this state of suspended animation, which was then reversed, and the animals were observed for 6 weeks. Cognitive functions were tested by training animals to retrieve food from color-coded boxes. Postoperatively, the ability to remember this task and a 75-point objective neurologic scale were used to test neurologic function. In experiment I, ULH was caused by lacerating thoracic aorta (n = 9). Five preoperatively untrained animals were trained to perform the task and compared with control animals (n = 15), and 4 preoperatively trained animals were tested for memory retention postoperatively. In experiment II, ULH was induced by creating an iliac artery and vein injury (n = 15). Animals were kept in shock for 15, 30, and 60 minutes before the induction of hypothermia.Results. In experiment I, surviving animals (719) were neurologically intact, and their capacity to learn new skills was no different than for control animals. All pretrained animals demonstrated complete memory retention. In experiment II, survival with 15, 30, and 60 minutes of shock were 80%, 60% and 80%, respectively. All animals (except 1) in the 60-minute group were neurologically intact and displayed normal learning capacity.Conclusions. Induction of hypothermic metabolic arrest (by thoracotomy) for repair of complex traumatic injuries is feasible with preservation of normal neurologic function, even after extended periods of shock from an intra-abdominal source of uncontrolled hemorrhage.