Huet O, Kinirons B, Dupic L, Lajeunie E, Mazoit J X, Benhamou D, Vicaut E, Duranteau J
Université Paris XI, Département d'Anesthésie Réanimation, Hôpital Bicêtre, Le Kremlin Bicêtre, France.
Acta Anaesthesiol Scand. 2007 Oct;51(9):1211-6. doi: 10.1111/j.1399-6576.2007.01419.x.
Hypothermia has been proposed as a therapeutic possibility in brain trauma, cardiac arrest and hemorrhagic shock. Experimental studies have shown that hypothermia may act by modulating the inflammatory response during endotoxemia. This study was carried out to test whether hypothermia could protect rats from endotoxemic insult.
After general anesthesia and oro-tracheal intubation, Sprague-Dawley rats were randomly assigned to either a hypothermic group or normothermic group. In each group, rats received intraperitoneal lipopolysaccharide (LPS) (10 or 20 mg/kg). Blood samples were taken prior to and 2 h after LPS injection to measure blood gases, liver enzymes, muscular enzymes, tumor necrosis factor-alpha (TNF-alpha) and interleukin-10 (IL-10) plasma levels. After 2 h of hypothermia, the rats were extubated and brought back to their cages. The mortality rate was observed for 7 days following endotoxemia. In a second set of experiments, hypothermia was induced 1 h after endotoxemia (10 mg/kg of intraperitoneal LPS) and the mortality rate was observed for the following 7 days.
The survival rate was significantly increased in the hypothermic group relative to the normothermic group, regardless of LPS dose. This increased survival rate was also observed when hypothermia was induced 1 h after endotoxemia. In the hypothermic group, IL-10 and the DeltaIL-10/DeltaTNF-alpha ratio were significantly increased relative to those in the normothermic group.
Induced mild hypothermia reduces mortality during endotoxemia in rats. The modulation of the inflammatory response, with an increase in anti-inflammatory cytokines, may be involved in this protective effect.
低温已被提议作为脑外伤、心脏骤停和失血性休克的一种治疗可能性。实验研究表明,低温可能通过调节内毒素血症期间的炎症反应发挥作用。本研究旨在测试低温是否能保护大鼠免受内毒素血症的损伤。
在全身麻醉和经口气管插管后,将Sprague-Dawley大鼠随机分为低温组或常温组。每组大鼠腹腔注射脂多糖(LPS)(10或20mg/kg)。在注射LPS前及注射后2小时采集血样,以测量血气、肝酶、肌肉酶、肿瘤坏死因子-α(TNF-α)和白细胞介素-10(IL-10)的血浆水平。低温处理2小时后,将大鼠拔管并放回笼中。观察内毒素血症后7天的死亡率。在第二组实验中,在内毒素血症(腹腔注射10mg/kg LPS)1小时后诱导低温,并观察接下来7天的死亡率。
无论LPS剂量如何,低温组的存活率相对于常温组均显著提高。在内毒素血症1小时后诱导低温时,也观察到存活率增加。与常温组相比,低温组的IL-10和ΔIL-10/ΔTNF-α比值显著升高。
诱导轻度低温可降低大鼠内毒素血症期间的死亡率。抗炎细胞因子增加对炎症反应的调节可能参与了这种保护作用。