INSERM, U955, Créteil, France.
Circulation. 2011 Aug 23;124(8):901-11, 1-7. doi: 10.1161/CIRCULATIONAHA.111.039388. Epub 2011 Aug 1.
In animal models of cardiac arrest, the benefit afforded by hypothermia is closely linked to the rapidity of the decrease in body temperature after resuscitation. Because total liquid ventilation (TLV) with temperature-controlled perfluorocarbons induces a very rapid and generalized cooling, we aimed to determine whether this could limit the post-cardiac arrest syndrome in a rabbit model. We especially focused on neurological, cardiac, pulmonary, liver and kidney dysfunctions.
Anesthetized rabbits were submitted to either 5 or 10 minutes of untreated ventricular fibrillation. After cardiopulmonary resuscitation and resumption of a spontaneous circulation, the animals underwent either normothermic life support (control) or therapeutic hypothermia induced by TLV. The latter procedure decreased esophageal and tympanic temperatures to 32°C to 33°C within only 10 minutes. After rewarming, the animals submitted to TLV exhibited an attenuated neurological dysfunction and decreased mortality 7 days later compared with control. The neuroprotective effect of TLV was confirmed by a significant reduction in brain histological damages. We also observed limitation of myocardial necrosis, along with a decrease in troponin I release and a reduced myocardial caspase 3 activity, with TLV. The beneficial effects of TLV were directly related to the rapidity of hypothermia induction because neither conventional cooling (cold saline infusion plus external cooling) nor normothermic TLV elicited a similar protection.
Ultrafast cooling instituted by TLV exerts potent neurological and cardiac protection in an experimental model of cardiac arrest in rabbits. This could be a relevant approach to provide a global and protective hypothermia against the post-cardiac arrest syndrome.
在心脏骤停的动物模型中,低温所带来的益处与复律后体温下降的速度密切相关。由于全液体通气(TLV)与控温的全氟化碳结合可实现非常快速和广泛的降温,我们旨在确定这种方法是否可以在兔模型中限制心脏骤停后综合征。我们特别关注神经、心脏、肺、肝和肾功能障碍。
麻醉兔经历 5 或 10 分钟未经处理的心室颤动。心肺复苏和自主循环恢复后,动物接受常规体温支持(对照组)或 TLV 诱导的治疗性低温。后者程序仅在 10 分钟内将食管和鼓室温度降至 32°C 至 33°C。复温后,与对照组相比,接受 TLV 的动物表现出较轻的神经功能障碍和 7 天后较低的死亡率。TLV 的神经保护作用通过显著减少脑组织损伤得到证实。我们还观察到心肌坏死的限制,同时肌钙蛋白 I 释放减少和心肌半胱天冬酶 3 活性降低,TLV 有此作用。TLV 的有益作用与低温诱导的速度直接相关,因为常规冷却(冷盐水输注加外部冷却)或常规体温 TLV 均未引起类似的保护作用。
TLV 实施的超快降温在兔心脏骤停实验模型中发挥出强大的神经和心脏保护作用。这可能是一种提供针对心脏骤停后综合征的全局和保护作用的低温的相关方法。