Alam Hasan B, Bowyer Mark W, Koustova Elena, Gushchin Vadim, Anderson Daniel, Stanton Kathleen, Kreishman Peter, Cryer Chad M t, Hancock Timothy, Rhee Peter
Department of Surgery, Uniformed Services University of the Health Sciences, Bethesda, Md 20814, USA.
Surgery. 2002 Aug;132(2):278-88. doi: 10.1067/msy.2002.125787.
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.
Yorkshire swine (100 to 125 lb) underwent ULH before rapid intra-aortic infusion of a hypothermic (4 degrees C), hyperkalemic (70 mEq/L) organ preservation solution by a left thoracotomy. Cooling continued until core temperature reached 10 degrees C, 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.
In experiment I, surviving animals (7/9) 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.
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.
如果能在创伤患者中安全诱导,无血低温代谢停滞(假死状态)可为修复严重血管损伤提供宝贵时间。我们报告了一种在非控制性致死性出血(ULH)猪模型中实现此目的的新方法,该方法可保留学习能力和记忆。
约克夏猪(体重100至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)器官保存液之前经历ULH。持续降温直至核心体温达到10℃,并使用低流量体外循环维持60分钟。在这种假死状态下修复血管损伤,然后使其逆转,并观察动物6周。通过训练动物从颜色编码的盒子中获取食物来测试认知功能。术后,使用记住此任务的能力和75分的客观神经学量表来测试神经功能。在实验I中,通过撕裂胸主动脉导致ULH(n = 9)。将5只术前未训练的动物训练执行该任务并与对照动物(n = 15)比较,4只术前训练的动物术后测试记忆保留情况。在实验II中,通过造成髂动脉和静脉损伤诱导ULH(n = 15)。在诱导低温之前,动物分别处于休克状态15、30和60分钟。
在实验I中,存活的动物(7/9)神经功能完好,其学习新技能的能力与对照动物无异。所有预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分钟后的存活率分别为80%、60%和80%。60分钟组中的所有动物(除1只外)神经功能完好且显示出正常的学习能力。
即使在腹腔内非控制性出血导致长时间休克后,通过胸廓切开术诱导低温代谢停滞以修复复杂创伤性损伤是可行的,且能保留正常神经功能。