背景:在有限的临床前模型中,缺血后处理(IPoC)已被证明可以改善预后。由于停机时间通常是未知的,这种技术需要在一系列场景中进行研究。由于该工具限制了再灌注损伤,在短暂停搏和有限的缺血再灌注损伤后,可能会有有限的益处甚至伤害。
方法:18只雄性Wistar大鼠经历了7分钟的窒息停滞。随机分配到IPoC的动物接受了20s的暂停,然后进行了20s的按压,重复四次,开始心肺复苏40秒。如果恢复了自主循环(ROSC),肾上腺素滴定至平均动脉压(MAP)为70mmHg。使用t检验或Mann-Whitney检验分析数据。显著性设置为p≤0.05。
结果:两组的ROSC率相当,88%。ROSC时间差异无统计学意义,ROSC后需要肾上腺素,颈动脉血流,或在任何时间点达到乳酸峰值。IPoC的MAP明显升高,90.7mmHg(SD13.9),与标准心肺复苏相比,76.7mmHg(8.5),ROSC后2小时,p=0.03。
结论:IPoC在大鼠模型中使用基于CPR的IPoC干预的新的停搏病因,在短期停搏模型中没有损害。
BACKGROUND: Ischemic post-conditioning (IPoC) has been shown to improve outcomes in limited pre-clinical models. As down-time is often unknown, this technique needs to be investigated over a range of scenarios. As this tool limits reperfusion injury, there may be limited benefit or even harm after short arrest and limited ischemia-reperfusion injury.
METHODS: Eighteen male Wistar rats underwent 7 min of asphyxial arrest. Animals randomized to IPoC received a 20 s pause followed by 20 s of compressions, repeated four times, initiated 40 s into cardiopulmonary resuscitation. If return of spontaneous circulation (ROSC) was achieved, epinephrine was titrated to mean arterial pressure (MAP) of 70 mmHg. Data were analyzed using t-test or Mann-Whitney test. Significance set at p ≤ 0.05.
RESULTS: The rate of ROSC was equivalent in both groups, 88%. There was no statistically significant difference in time to ROSC, epinephrine required post ROSC, carotid flow, or peak lactate at any timepoint. There was a significantly elevated MAP with IPoC, 90.7 mmHg (SD 13.9), as compared to standard CPR, 76.7 mmHg (8.5), 2 h after ROSC, p = 0.03.
CONCLUSIONS: IPoC demonstrated no harm in a model of short arrest using a new arrest etiology for CPR based IPoC intervention in a rat model.