Seventy-two hours of mild hypothermia after cardiac arrest is associated with a lowered inflammatory response during rewarming in a prospective observational study

Introduction

Whole-body ischemia and reperfusion trigger a systemic inflammatory response. In this study, we analyzed the effect of temperature on the inflammatory response in patients treated with prolonged mild hypothermia after cardiac arrest.

Methods

Ten comatose patients with return of spontaneous circulation after pulseless electrical activity/asystole or prolonged ventricular fibrillation were treated with mild therapeutic hypothermia for 72 hours after admission to a tertiary care university hospital. At admission and at 12, 24, 36, 48, 72, 96 and 114 hours, the patients’ temperature was measured and blood samples were taken from the arterial catheter. Proinflammatory interleukin 6 (IL-6) and anti-inflammatory (IL-10) cytokines and chemokines (IL-8 and monocyte chemotactic protein 1), intercellular adhesion molecule 1 and complement activation products (C1r-C1s-C1inhibitor, C4bc, C3bPBb, C3bc and terminal complement complex) were measured. Changes over time were analyzed with the repeated measures test for nonparametric data. Dunn’s multiple comparisons test was used for comparison of individual time points.

Results

The median temperature at the start of the study was 34.3°C (33.4°C to 35.2°C) and was maintained between 32°C and 34°C for 72 hours. All patients were passively rewarmed after 72 hours, from (median (IQR)) 33.7°C (33.1°C to 33.9°C) at 72 hours to 38.0°C (37.5°C to 38.1°C) at 114 hours (P <0.001). In general, the cytokines and chemokines remained stable during hypothermia and decreased during rewarming, whereas complement activation was suppressed during the whole hypothermia period and increased modestly during rewarming.

Conclusions

Prolonged hypothermia may blunt the inflammatory response after rewarming in patients after cardiac arrest. Complement activation was low during the whole hypothermia period, indicating that complement activation is also highly temperature-sensitive in vivo. Because inflammation is a strong mediator of secondary brain injury, a blunted proinflammatory response after rewarming may be beneficial.     

不同诱导方法诱导家蝇幼虫血淋巴中抗菌肽差异性的SDS-PAGE检测

目的 检测不同诱导方法(针刺,紫外,热诱导)诱导家蝇三龄幼虫血淋巴中的抗茵肽的差异性.方法 用不同诱导方法诱导家蝇三龄幼虫,提取血淋巴后,采用梯度乙腈洗脱,应用SDS-PAGE检测抗菌肽的差异性.结果 针刺与未诱导组无明显差异,热诱导组中30%乙腈洗脱组分中在30～71 KD中出现3个差异条带,紫外诱导组50%乙腈洗脱组分在16～20 KD中出现2个差异条带,60%乙腈洗脱组分中在16-20 KD中出现2个差异条带.结论 综合幼虫的成活率及操作的方便性,最佳的诱导方法为热诱导.     

注射用尤瑞克林治疗急性脑梗死的临床疗效观察

目的 观察尤瑞克林治疗急性脑梗死的临床疗效.方法 将符合入选条件的60例急性脑梗死惠者分为治疗组和对照组,每组30例.两组基础治疗相似,治疗组患者加用尤瑞克林,每日1次;分别给予治疗前后神经功能缺损评分和临床疗效比较,同时检测血常规、尿常规、肝肾功能及凝血功能等.结果 治疗组神经功能缺损评分较治疗前差异有统计学意义(P<0.05),疗效明显优于对照组,且无不良反应.结论 尤瑞克林治疗急性脑梗死疗效确切,安全可靠.