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Biomedical responses to changes in body temperature in ciritically ill patients

危重病人体温变化的生物医学反应

基本信息

批准号：
10470248
负责人：
AIKAWA Naoki
金额：
$ 8.19万
依托单位：
Keio University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (B)
财政年份：
1998
资助国家：
日本
起止时间：
1998 至 1999
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/grant/KAKENHI-PROJECT-10470248/
关键词：
interleukin-8 cytokine body temperature whole blood culture hypothermia hyperthermia TNFα IL-6

项目摘要

We initially measured the plasma levels of cytokines, soluble receptors and examined their relationships to the degree of systemic infection and body temperature. In the presence of apparent infection, the plasma IL-6 and IL-8 levels were significantly increased. We found a significant correlation between body temperature and TNF-alpha, IL-6 and IL-8. We then analyzed the hyperthermic patients, whose consciousness was transiently disturbed and who did not show any signs of infection, and found that the plasma levels of IL-6, IL-8 and IL-10 were initially high and then decreased gradually, These data suggested that hyperthermia itself could induce the production of cytokines.In the second experiment, we examined the effect of environmental temperature on IL-8 production in heparinized whole blood in vitro. Small volume of IL-8 was produced without any stimuli. Interestingly, IL-8 production, in response to endotoxin was rather inhibited when incubated at 42℃, 40℃, but not at 38℃. In combination with above in vivo findings, we speculated that cytokine or cytokine-stimulating factor may be produced by no hematological cells in hyperthermic patients. Additionally, we have made a system for future analysis of cell functions, such as calcium response, cell surface markers, etc.

我们首先测量了血浆中细胞因子和可溶性受体的水平，并研究了它们与全身感染程度和体温的关系。在存在明显感染的情况下，血浆IL-6和IL-8水平显著升高。我们发现体温与TNF-α、IL-6和IL-8之间存在显著相关性。然后我们分析了体温过高患者，他们的意识暂时受到干扰，没有任何感染迹象，发现血浆IL-6，IL-8和IL-10水平最初很高，然后逐渐下降，这些数据表明体温过高本身可以诱导细胞因子的产生。我们检测了环境温度对体外肝素化全血中IL-8产生的影响。在没有任何刺激的情况下产生小体积的IL-8。有趣的是，当在42℃、40℃下孵育时，响应于内毒素的IL-8的产生受到相当程度的抑制，但在38℃下不受抑制。结合上述体内实验结果，我们推测高热病人的血液细胞可能无细胞因子或促肾上腺素生成因子的产生。此外，我们还建立了一个系统，用于未来分析细胞功能，如钙反应，细胞表面标记物等。