Beurskens Charlotte J, Horn Janneke, de Boer Anita M Tuip, Schultz Marcus J, van Leeuwen Ester Mm, Vroom Margreeth B, Juffermans Nicole P
Crit Care. 2014 Jul 30;18(4):R162. doi: 10.1186/cc14002.
Induced hypothermia is increasingly applied as a therapeutic intervention in ICUs. One of the underlying mechanisms of the beneficial effects of hypothermia is proposed to be reduction of the inflammatory response. However, a fear of reducing the inflammatory response is an increased infection risk. Therefore, we studied the effect of induced hypothermia on immune response after cardiac arrest.
A prospective observational cohort study in a mixed surgical-medical ICU. Patients admitted at the ICU after surviving cardiac arrest were included and during 24 hours body temperature was strictly regulated at 33°C or 36°C. Blood was drawn at three time points: after reaching target temperature, at the end of the target temperature protocol and after rewarming to 37°C. Plasma cytokine levels and response of blood leucocytes to stimulation with toll-like receptor (TLR) ligands lipopolysaccharide (LPS) from Gram-negative bacteria and lipoteicoic acid (LTA) from Gram-positive bacteria were measured. Also, monocyte HLA-DR expression was determined.
In total, 20 patients were enrolled in the study. Compared to healthy controls, cardiac arrest patients kept at 36°C (n = 9) had increased plasma cytokines levels, which was not apparent in patients kept at 33°C (n = 11). Immune response to TLR ligands in patients after cardiac arrest was generally reduced and associated with lower HLA-DR expression. Patients kept at 33°C had preserved ability of immune cells to respond to LPS and LTA compared to patients kept at 36°C. These differences disappeared over time. HLA-DR expression did not differ between 33°C and 36°C.
Patients after cardiac arrest have a modest systemic inflammatory response compared to healthy controls, associated with lower HLA-DR expression and attenuated immune response to Gram-negative and Gram-positive antigens, the latter indicative of an impaired immune response to bacteria. Patients with a body temperature of 33°C did not differ from patients with a body temperature of 36°C, suggesting induced hypothermia does not affect immune response in patients with cardiac arrest.
ClinicalTrials.gov NCT01020916, registered 25 November 2009.
亚低温诱导作为一种治疗手段在重症监护病房（ICU）中的应用日益广泛。低温有益作用的潜在机制之一被认为是炎症反应的减轻。然而，人们担心炎症反应的减轻会增加感染风险。因此，我们研究了亚低温诱导对心脏骤停后免疫反应的影响。
在一所外科与内科混合的ICU中进行一项前瞻性观察队列研究。纳入在心脏骤停后存活并入住该ICU的患者，在24小时内将体温严格控制在33°C或36°C。在三个时间点采血：达到目标温度后、目标温度方案结束时以及复温至37°C后。检测血浆细胞因子水平以及血液白细胞对来自革兰氏阴性菌的脂多糖（LPS）和来自革兰氏阳性菌的脂磷壁酸（LTA）等Toll样受体（TLR）配体刺激的反应。此外，还测定了单核细胞人类白细胞抗原-DR（HLA-DR）的表达。
总共20名患者纳入本研究。与健康对照相比，体温维持在36°C的心脏骤停患者（n = 9）血浆细胞因子水平升高，而体温维持在33°C的患者（n = 11）则不明显。心脏骤停患者对TLR配体的免疫反应普遍降低，并与较低的HLA-DR表达相关。与体温维持在36°C的患者相比，体温维持在33°C的患者免疫细胞对LPS和LTA的反应能力得以保留。这些差异随时间消失。33°C和36°C时HLA-DR表达无差异。
与健康对照相比，心脏骤停患者存在适度的全身炎症反应，与较低的HLA-DR表达以及对革兰氏阴性和革兰氏阳性抗原的免疫反应减弱相关，后者表明对细菌的免疫反应受损。体温为33°C的患者与体温为36°C的患者无差异，提示亚低温诱导不影响心脏骤停患者的免疫反应。
ClinicalTrials.gov NCT01020916，于2009年11月25日注册。
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