Qadan Motaz, Gardner Sarah A, Vitale David S, Lominadze David, Joshua Irving G, Polk Hiram C
Price Institute of Surgical Research, University of Louisville School of Medicine, Medical-Dental Research Building (3rd Floor), 511 South Floyd St, Louisville, Kentucky 40202, USA.
Ann Surg. 2009 Jul;250(1):134-40. doi: 10.1097/SLA.0b013e3181ad85f7.
To examine cellular and immunologic mechanisms by which intraoperative hypothermia affects surgical patients.
Avoidance of perioperative hypothermia has recently become a focus of attention as an important quality performance measure, aimed at optimizing the care of surgical patients. Anesthetized surgical patients are particularly at risk for hypothermia, which has been directly linked to the development of sequelae, such as coagulopathy, infection, morbid myocardial events, and death after surgery. However, many of the underlying immunologic mechanisms remain unclear.
Venous blood samples from healthy volunteers were exposed for up to 4 hours to various temperatures following the addition of a 1 ng/mL lipopolysaccharide challenge. Innate immune function, assessed by the ability of monocytes to present antigen and coordinate cytokine release, was determined by qualitative and quantitative measurements of HLA-DR surface expression 2 hours following incubation, and proinflammatory tumor necrosis factor-alpha (TNF-alpha) and anti-inflammatory (IL-10) cytokine release in the first 4 hours.
Monocyte incubation at hypothermic temperatures (34 degrees C) reduced HLA-DR surface expression, delayed TNF-alpha clearance, and increased IL-10 release. Conversely, hyperthermia (40 degrees C) increased monocyte antigen presentation and resulted in rapid decay of TNF-alpha. However, IL-10 release was also increased. Normothermia (37 degrees C) attenuated IL-10 release following the initial proinflammatory surge.
Hypothermia exerts multiple effects at the cellular level, which impair innate immune function, and are associated with increased septic complications and mortality. These findings provide a physiological basis for perioperative temperature monitoring, which is a valid surgical performance measure that can be used to reduce surgical complications associated with avoidable hypothermia.
研究术中低温影响手术患者的细胞和免疫机制。
避免围手术期低温最近已成为关注焦点,作为一项重要的质量绩效指标,旨在优化手术患者的护理。麻醉的手术患者尤其易发生低温,这与诸如凝血病、感染、严重心肌事件及术后死亡等后遗症的发生直接相关。然而,许多潜在的免疫机制仍不清楚。
在添加1 ng/mL脂多糖刺激后,将健康志愿者的静脉血样本暴露于不同温度下长达4小时。通过单核细胞呈递抗原和协调细胞因子释放的能力评估固有免疫功能,在孵育2小时后通过定性和定量测量HLA-DR表面表达来确定,并在前4小时测量促炎肿瘤坏死因子-α(TNF-α)和抗炎(IL-10)细胞因子的释放。
在低温(34摄氏度)下孵育单核细胞会降低HLA-DR表面表达,延迟TNF-α清除,并增加IL-10释放。相反,高温(40摄氏度)会增加单核细胞抗原呈递并导致TNF-α快速衰减。然而,IL-10释放也会增加。正常体温(37摄氏度)会在最初的促炎激增后减弱IL-10释放。
低温在细胞水平上产生多种影响,损害固有免疫功能,并与脓毒症并发症和死亡率增加相关。这些发现为围手术期体温监测提供了生理基础,这是一项有效的手术绩效指标,可用于减少与可避免的低温相关的手术并发症。