Department of Anesthesiology and Critical Care Medicine, Johns Hopkins University, Baltimore, Maryland, United States.
Department of Medicine, Johns Hopkins University, Baltimore, Maryland, United States.
Am J Physiol Regul Integr Comp Physiol. 2024 Sep 1;327(3):R304-R318. doi: 10.1152/ajpregu.00078.2024. Epub 2024 Jun 11.
Clinical trials of hypothermia after pediatric cardiac arrest (CA) have not seen robust improvement in functional outcome, possibly because of the long delay in achieving target temperature. Previous work in infant piglets showed that high nasal airflow, which induces evaporative cooling in the nasal mucosa, reduced regional brain temperature uniformly in half the time needed to reduce body temperature. Here, we evaluated whether initiation of hypothermia with high transnasal airflow provides neuroprotection without adverse effects in the setting of asphyxic CA. Anesthetized piglets underwent sham-operated procedures ( = 7) or asphyxic CA with normothermic recovery (38.5°C; = 9) or hypothermia initiated by surface cooling at 10 ( = 8) or 120 ( = 7) min or transnasal cooling initiated at 10 ( = 7) or 120 ( = 7) min after resuscitation. Hypothermia was sustained at 34°C with surface cooling until 20 h followed by 6 h of rewarming. At 4 days of recovery, significant neuronal loss occurred in putamen and sensorimotor cortex. Transnasal cooling initiated at 10 min significantly rescued the number of viable neurons in putamen, whereas levels in putamen in other hypothermic groups remained less than sham levels. In sensorimotor cortex, neuronal viability in the four hypothermic groups was not significantly different from the sham group. These results demonstrate that early initiation of high transnasal airflow in a pediatric CA model is effective in protecting vulnerable brain regions. Because of its simplicity, portability, and low cost, transnasal cooling potentially could be deployed in the field or emergency room for early initiation of brain cooling after pediatric CA. The onset of therapeutic hypothermia after cardiac resuscitation is often delayed, leading to incomplete neuroprotection. In an infant swine model of asphyxic cardiac arrest, initiation of high transnasal airflow to maximize nasal evaporative cooling produced hypothermia sufficient to provide neuroprotection that was not inferior to body surface cooling. Because of its simplicity and portability, this technique may be of use in the field or emergency room for rapid brain cooling in pediatric cardiac arrest victims.
儿科心搏骤停（CA）后的低温临床试验并未看到功能预后的显著改善，这可能是由于达到目标温度的时间过长。之前在婴儿猪模型中的研究表明，高鼻气流通过诱导鼻黏膜蒸发冷却，可以在一半的时间内均匀降低局部脑温，所需时间比降低体温所需时间更短。在这里，我们评估了在缺氧性 CA 中，使用高经鼻气流开始低温治疗是否可以提供神经保护而无不良影响。麻醉后的小猪接受假手术程序（n = 7）或正常体温恢复的缺氧性 CA（38.5°C；n = 9）或低温治疗，低温治疗通过表面冷却在复苏后 10（n = 8）或 120（n = 7）分钟开始，或通过经鼻冷却在复苏后 10（n = 7）或 120（n = 7）分钟开始。通过表面冷却将体温维持在 34°C 直至 20 小时，随后进行 6 小时复温。在恢复的第 4 天，壳核和感觉运动皮层出现明显的神经元丢失。在复苏后 10 分钟开始的经鼻冷却显著挽救了壳核中存活神经元的数量，而其他低温治疗组的壳核水平仍低于假手术组。在感觉运动皮层中，四个低温治疗组的神经元存活率与假手术组无显著差异。这些结果表明，在儿科 CA 模型中早期开始高经鼻气流是有效保护易损脑区的。由于其简单性、便携性和低成本，经鼻冷却有可能在现场或急诊室用于在儿科 CA 后早期开始脑冷却。心脏复苏后治疗性低温的开始往往会延迟，导致不完全的神经保护。在缺氧性心脏骤停的婴儿猪模型中，启动高鼻气流以最大限度地增加鼻蒸发冷却可产生足够的低温以提供不劣于体表冷却的神经保护。由于其简单性和便携性，该技术可能在现场或急诊室用于儿科心脏骤停患者的快速脑冷却。
