Short-term, Mild Hypothermia Can Increase the Beneficial Effect of Permissive Hypotension on Uncontrolled Hemorrhagic Shock in Rats

Short-term, Mild Hypothermia Can Increase the Beneficial Effect of Permissive Hypotension on Uncontrolled Hemorrhagic Shock in Rats
复制标题

短期轻度低温可以增加允许性低血压对失血性休克大鼠的有益作用

DOI:
10.1097/aln.0b013e318256f09d
复制
发表时间:
2012-06-01
期刊:
影响因子:
8.8
通讯作者:
Liu, Liangming
Liu, Liangming
中科院分区:
医学1区
文献类型:
--
作者:
Li, Tao;Lin, Xiulai;Liu, Liangming

文献摘要

被引文献

相似文献

背景:我们之前和其他研究表明,低血压或低温复苏对失血性休克失血性休克具有有益作用。低温是否可以增加低血压复苏对失血性休克的有益效果尚不清楚。方法:220只Sprague-Dawley大鼠被用来制造失血性休克。在出血得到控制之前,大鼠接受正常血压或低血压复苏(目标平均动脉压为 80 或 50 mmHg)并结合正常体温 (37°C) 或轻度低温 (34°C)(II 期)。出血控制后,大鼠接受全血和乳酸林格氏溶液复苏2小时(III期)。记录动物的存活、失血量、液体需求、心输出量和凝血功能,以及重要器官功能、线粒体功能和肝、肾和肠的能量代谢。结果:出血控制前的短期轻度低温增加了低血压复苏的有益效果。低温进一步减少了低血压复苏过程中的失血量、耗氧量以及肝、肾、肠道的功能损伤,保护了线粒体功能和能量代谢(Na+-K+-ATPase活性),进一步提高了生存时间和生存率(低温/低压联合组:生存率,9/10;生存时间,616 min;常温/常压组:1/10,256 min;低温/正常血压组:4/10,293 分钟)。低温轻度抑制凝血功能。结论:出血控制前的亚低温可以增加低血压复苏对失血性休克失血性休克的治疗效果。短期低温获益的机制可能与氧消耗和代谢的减少以及线粒体和器官功能的保护有关。
Background: Our previous and other studies have shown that hypotensive or hypothermic resuscitation have beneficial effects on uncontrolled hemorrhagic shock. Whether hypothermia can increase the beneficial effect of hypotensive resuscitation on hemorrhagic shock is not known. Methods: Two-hundred and twenty Sprague-Dawley rats were used to make uncontrolled hemorrhagic shock. Before bleeding was controlled, rats received normotensive or hypotensive resuscitation (target mean arterial pressure at 80 or 50 mmHg) in combination with normal (37°C) or mild hypothermia (34°C) (phase II). After bleeding was controlled, rats received whole blood and lactated Ringer's solution resuscitation for 2 h (phase III). The animal survival, blood loss, fluid requirement, cardiac output, and coagulation functions, as well as vital organ function, mitochondrial function, and energy metabolism of liver, kidney and intestines, were noted. Results: Short-term, mild hypothermia before bleeding was controlled increased the beneficial effect of hypotensive resuscitation. Hypothermia further decreased blood loss, oxygen consumption, and functional damage to the liver, kidney, and intestines during hypotensive resuscitation, protected mitochondrial function and energy metabolism (activity of Na+-K+-ATPase), and further improved survival time and survival rate (hypothermic/hypotensive combined group: survival rate, 9/10; survival time, 616 min; normothermic/normotensive group: 1/10, 256 min; hypothermic/normotensive group: 4/10, 293 min). Hypothermia slightly inhibited coagulation function. Conclusion: Mild hypothermia before bleeding is controlled can increase the beneficial effect of hypotensive resuscitation on uncontrolled hemorrhagic shock. The mechanism underlying the benefits of short-term hypothermia may be related to the decrease in oxygen consumption and metabolism, and protection of mitochondrial and organ functions.