Swoboda Stefanie, Gruettner Joachim, Lang Siegfried, Wendel Hans-Peter, Beyer Martin E, Griesel Eva, Hoffmeister Hans-Martin, Walter Thomas
Pharmacy Department of the University Hospital of Heidelberg, Heidelberg, Germany.
Emergency Department, University Medical Center Mannheim, Medical Faculty Mannheim, Heidelberg University, Mannheim, Germany.
Exp Ther Med. 2014 Aug;8(2):488-492. doi: 10.3892/etm.2014.1737. Epub 2014 May 28.
Deep hypothermic circulatory arrest (DHCA) is a common technique used to protect vital organs during surgical interventions on the thoracic aorta or during surgery for complex congenital heart disease. Activated leukocytes are key mediators of inflammatory responses during ischemia. Intercellular crosstalk between leukocytes, platelets and endothelial cells is mediated by cell adhesion molecules. These molecules trigger complex cell-cell interaction mechanisms and initiate the release of proinflammatory molecules. One parameter that is known to have a significant impact on inflammatory cell activation and the production of proinflammatory markers is temperature. However, to the best of our knowledge, no data have yet been published on the effect of hypothermia on leukocyte surface markers during DHCA. Thus, the aim of the present study was to investigate the effect of hypothermia on the expression of cell adhesion molecules on monocytes under DHCA conditions . Blood samples collected from 11 healthy volunteers were incubated in a well-established model simulating circulatory arrest at 36°C and 18°C for 30 min. The expression of cluster of differentiation (CD) molecule 11B (CD11b), CD54 and CD162 on monocytes was measured as the mean fluorescence intensity (MFI) using flow cytometry. The expression level of CD11b on monocytes was significantly decreased following the incubation of the blood samples at 18°C compared with the level in blood samples incubated at 36°C (P<0.001). After 30 min of blood stasis in the circulatory arrest model, the expression level of CD162 on monocytes was significantly lower in the blood samples incubated at 18°C than in those incubated at 36°C (P<0.001). No association was identified between temperature and the surface expression of CD54 on monocytes following 30 min of stasis. These findings demonstrate that deep hypothermia decreases the expression of CD11b and CD162 on monocytes in an experimental setup simulating the conditions of DHCA. This may be the result of the inhibition of leukocyte-endothelial and leukocyte-platelet interactions, which may be a beneficial aspect of deep hypothermia that affects the inflammatory response and tissue damage during DHCA.
深低温停循环（DHCA）是一种在胸主动脉手术干预或复杂先天性心脏病手术期间用于保护重要器官的常用技术。活化的白细胞是缺血期间炎症反应的关键介质。白细胞、血小板和内皮细胞之间的细胞间串扰由细胞粘附分子介导。这些分子触发复杂的细胞间相互作用机制并引发促炎分子的释放。已知对炎症细胞活化和促炎标志物产生有重大影响的一个参数是温度。然而，据我们所知，尚未有关于低温对DHCA期间白细胞表面标志物影响的数据发表。因此，本研究的目的是研究低温对DHCA条件下单核细胞上细胞粘附分子表达的影响。从11名健康志愿者采集的血样在模拟36°C和18°C循环骤停的成熟模型中孵育30分钟。使用流式细胞术将单核细胞上分化簇（CD）分子11B（CD11b）、CD54和CD162的表达测量为平均荧光强度（MFI）。与在36°C孵育的血样相比，在18°C孵育血样后，单核细胞上CD11b的表达水平显著降低（P<0.001）。在循环骤停模型中血液淤积30分钟后，在18°C孵育的血样中单核细胞上CD162的表达水平明显低于在36°C孵育的血样（P<0.001）。在血液淤积30分钟后，未发现温度与单核细胞上CD54的表面表达之间存在关联。这些发现表明，在模拟DHCA条件的实验装置中，深低温会降低单核细胞上CD11b和CD162的表达。这可能是白细胞-内皮细胞和白细胞-血小板相互作用受到抑制的结果，这可能是深低温影响DHCA期间炎症反应和组织损伤的一个有益方面。
