Effects of the duration of postresuscitation hyperoxic ventilation on neurological outcome and survival in an asphyxial cardiac arrest rat model
Effects of the duration of postresuscitation hyperoxic ventilation on neurological outcome and survival in an asphyxial cardiac arrest rat model
复制标题
复苏后高氧通气持续时间对窒息心脏骤停大鼠模型神经功能结局和生存的影响
DOI：
10.1038/s41598-019-52477-y
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发表时间：
2019-11-11
影响因子：
4.6
通讯作者：
Li, Yongqin
中科院分区：
文献类型：
--
作者：
Hu, Tongyi;Wang, Jianjie;Li, Yongqin
心脏骤停导致氧气供应突然停止，当大脑供氧不足时发生脑缺氧。现行成人心肺复苏（CPR）和心血管急救指南建议在复苏过程中使用100%的氧气，以最大限度地提高实现自然循环恢复（ROSC）的可能性。然而，ROSC后氧管理的最佳策略仍存在争议。本研究的目的是评估复苏后高氧通气持续时间对采用靶向温度管理（TTM）治疗的窒息性心脏骤停大鼠神经预后的影响。80只成年雄性Sprague-Dawley大鼠气管内插管阻断致窒息。未经治疗的心脏骤停7分钟后开始心肺复苏术。将动物随机分为常温对照组（NNC），或ROSC后立即分为4个实验组（每个实验组n = 16）： 100%氧气通气0 （O2_0h）、1 （O2_1h）、3 （O2_3h）或5 (O2_5h) h，然后在TTM下使用室内空气通气。在基线和复苏后6小时监测期间记录生理变量。密切观察动物96小时，评估神经恢复和生存。各组之间基线测量值无显著差异，所有动物均成功复苏。100%给氧时间与血流动力学以及心肌和脑损伤之间存在显著的相互作用。在研究的所有高氧通气时间中，o233h组的神经功能缺损评分明显低于NNC组，生存率明显高于NNC组。综上所述，复苏后高氧通气可改善窒息性心脏骤停大鼠的PaO2、PaCO2、血流动力学、心肌和脑恢复。然而，高浓度氧的有益作用是持续时间依赖的，在诱导低温期间100%氧通气有助于改善96小时后的神经恢复和生存。
Cardiac arrest leads to sudden cessation of oxygen supply and cerebral hypoxia occurs when there is not sufficient oxygen supplied to the brain. Current Guidelines for adult cardiopulmonary resuscitation (CPR) and emergency cardiovascular care recommend the use of 100% oxygen during resuscitative efforts to maximize the probability of achieving the return of spontaneous circulation (ROSC). However, the optimal strategy for oxygen management after ROSC is still debatable. The aim of the present study was to evaluate the effects of the duration of post-resuscitation hyperoxic ventilation on neurological outcomes in asphyxial cardiac arrest rats treated with targeted temperature management (TTM). Asphyxia was induced by blocking the endotracheal tube in 80 adult male Sprague-Dawley rats. CPR begun after 7 min of untreated cardiac arrest. Animals were randomized to either the normoxic control under normothermia (NNC) group or to one of the 4 experimental groups (n = 16 each) immediately after ROSC: ventilated with 100% oxygen for 0 (O2_0h), 1 (O2_1h), 3 (O2_3h), or 5 (O2_5h) h and ventilated with room air thereafter under TTM. Physiological variables were recorded at baseline and during the 6 h postresuscitation monitoring period. Animals were closely observed for 96 h to assess neurologic recovery and survival. There were no significant differences in baseline measurements between groups, and all animals were successfully resuscitated. There were significant interactions between the duration of 100% oxygen administration and hemodynamics as well as, myocardial and cerebral injuries. Among all the durations of hyperoxic ventilation investigated, significantly lower neurological deficit scores and higher survival rates were observed in the O2_3h group than in the NNC group. In conclusion, postresuscitation hyperoxic ventilation leads to improved PaO2, PaCO2, hemodynamic, myocardial and cerebral recovery in asphyxial cardiac arrest rats treated with TTM. However, the beneficial effects of high concentration-oxygen are duration dependent and ventilation with 100% oxygen during induced hypothermia contributes to improved neurological recovery and survival after 96 h.