Callaway Clifton W, Rittenberger Jon C, Logue Eric S, McMichael Melissa J
Department of Emergency Medicine, University of Pittsburgh, Pittsburgh, PA, USA.
Crit Care Med. 2008 Sep;36(9):2607-12. doi: 10.1097/CCM.0b013e318184443b.
Hypothermia improves survival and neurologic recovery after cardiac arrest. Cardiac arrest also triggers release of cytokines and inflammatory molecules, and it is unknown whether therapeutic hypothermia alters this inflammatory response. This study tested whether therapeutic hypothermia altered levels of inflammatory markers in serum.
Prospective, randomized study.
University research laboratory.
Adult, male, Sprague-Dawley rats.
Halothane-anesthetized rats were subjected to 8 mins of asphyxial cardiac arrest and resuscitation. Rat temperature was controlled at 37 degrees C throughout the experiment (normothermia) or reduced to 33 degrees C between 1 and 24 hrs after cardiac arrest (hypothermia). Serum cytokines were measured at baseline, 0.5, 1, 3, 6, 12, and 24 hrs after resuscitation using multiplex analyzer or enzyme-linked immunosorbent assay.
Hypothermic rats showed improved neurologic recovery at 12 and 24 hrs. Serum levels of tumor necrosis factor-alpha; macrophage inflammatory protein-1alpha; growth-related oncogene/keratinocyte chemokine; interleukin-2, -9, and -10; monocyte chemotactic protein-1; leptin; and intracellular adhesion molecule-1 increased over time, and the levels of interleukin-18 declined over time. No temporal trends in other molecules were detected. Levels of these molecules did not differ between temperature groups during the hypothermia phase (1-24 hrs).
These data suggest that altering the inflammatory response after cardiac arrest is not necessary for the beneficial effects of hypothermia. These data do not support a specific role of circulating cytokines in the neurologic injury after cardiac arrest.
低温可改善心脏骤停后的生存率和神经功能恢复。心脏骤停还会引发细胞因子和炎症分子的释放，目前尚不清楚治疗性低温是否会改变这种炎症反应。本研究测试了治疗性低温是否会改变血清中炎症标志物的水平。
前瞻性随机研究。
大学研究实验室。
成年雄性Sprague-Dawley大鼠。
用氟烷麻醉的大鼠经历8分钟的窒息性心脏骤停及复苏。在整个实验过程中，大鼠体温控制在37℃（正常体温），或在心脏骤停后1至24小时降至33℃（低温）。使用多重分析仪或酶联免疫吸附测定法在复苏后基线、0.5、1、3、6、12和24小时测量血清细胞因子。
低温组大鼠在12和24小时时神经功能恢复情况有所改善。肿瘤坏死因子-α、巨噬细胞炎性蛋白-1α、生长相关癌基因/角质形成细胞趋化因子、白细胞介素-2、-9和-及-10、单核细胞趋化蛋白-1、瘦素和细胞间黏附分子-1的血清水平随时间升高，而白细胞介素-18水平随时间下降。未检测到其他分子的时间趋势。在低温阶段（1至24小时），这些分子的水平在不同温度组之间没有差异。
这些数据表明，改变心脏骤停后的炎症反应对于低温的有益作用并非必要。这些数据不支持循环细胞因子在心脏骤停后神经损伤中起特定作用。
