Heidemann S M, Lomo L, Ofenstein J P, Sarnaik A P
Department of Pediatrics, Children's Hospital of Michigan, Wayne State University School of Medicine, Detroit, USA.
Crit Care Med. 2000 May;28(5):1465-8. doi: 10.1097/00003246-200005000-00035.
To determine whether heat stress protects the endotoxemic rat by up-regulation of the counterinflammatory cytokine interleukin (IL)-10, thereby attenuating the inflammatory response.
A total of 16 rats were assigned to either the heat stress group (n = 8) or the control group (n = 8). The heat stress group was warmed to a temperature of >42 degrees C (107.6 degrees F) rectally for 10-15 mins; 20 hrs later, all rats were intubated, paralyzed, and ventilated. After jugular venous and arterial catheterization, endotoxin was given intravenously. Arterial blood was removed at 0, 2, 4, and 5 hrs for blood gases, tumor necrosis factor (TNF)-alpha, nitric oxide metabolites (NO), IL-10, and macrophage inflammatory protein (MIP)-2. The alveolar macrophages were removed, counted, and then incubated for 24 hrs. The supernatant was analyzed for TNF-alpha, NO, IL-10, and MIP-2.
University research laboratory.
Male Sprague-Dawley rats (n = 16).
Administration of heat before endotoxin infusion.
Alveolar-arterial oxygen gradient was lower in the heat stress group at 4 and 5 hrs after endotoxemia. Plasma and alveolar macrophage supernatant concentrations of TNF-alpha, NO, and IL-10 were not affected by heat. Plasma and alveolar macrophage supernatant MIP-2 concentrations were higher in endotoxemic rats receiving heat pretreatment compared with controls.
Our study demonstrates that heat leads to pulmonary protection of short duration in severe endotoxemia. This protection was not mediated by plasma TNF-alpha, IL-10, or NO. Contrary to our hypothesis, pretreatment with heat increased rather than decreased the plasma MIP-2 concentration and alveolar macrophage production of MIP-2 in endotoxemia. The mechanism of heat-conferred pulmonary protection in endotoxemia remains unclear. Alveolar macrophages do not produce IL-10 in endotoxemia. The increased MIP-2 production by heated alveolar macrophages was not attributable to alterations in production of either TNF-alpha or IL-10. The significance of increased MIP-2 by endotoxin-exposed alveolar macrophages in heated rats is unknown.
确定热应激是否通过上调抗炎细胞因子白细胞介素（IL）-10来保护内毒素血症大鼠，从而减轻炎症反应。
总共16只大鼠被分为热应激组（n = 8）或对照组（n = 8）。热应激组大鼠经直肠加热至体温>42摄氏度（107.6华氏度），持续10 - 15分钟；20小时后，所有大鼠均进行气管插管、麻痹并机械通气。在颈静脉和动脉插管后，静脉注射内毒素。在0、2、4和5小时采集动脉血，检测血气、肿瘤坏死因子（TNF）-α、一氧化氮代谢产物（NO）、IL-10和巨噬细胞炎性蛋白（MIP）-2。取出肺泡巨噬细胞，计数，然后培养24小时。分析培养上清液中的TNF-α、NO、IL-10和MIP-2。
大学研究实验室。
雄性Sprague-Dawley大鼠（n = 16）。
在内毒素输注前进行热预处理。
内毒素血症后4小时和5小时，热应激组的肺泡-动脉氧分压差较低。热预处理对血浆和肺泡巨噬细胞上清液中TNF-α、NO和IL-10的浓度无影响。与对照组相比，接受热预处理的内毒素血症大鼠血浆和肺泡巨噬细胞上清液中的MIP-2浓度更高。
我们的研究表明，热应激可在严重内毒素血症中产生短期的肺保护作用。这种保护作用不是由血浆TNF-α、IL-10或NO介导的。与我们的假设相反，热预处理增加而非降低了内毒素血症大鼠血浆MIP-2浓度以及肺泡巨噬细胞MIP-2的产生。热应激在内毒素血症中赋予肺保护作用的机制尚不清楚。内毒素血症时肺泡巨噬细胞不产生IL-10。热刺激的肺泡巨噬细胞MIP-2产生增加并非归因于TNF-α或IL-10产生的改变。内毒素暴露的肺泡巨噬细胞在热刺激大鼠中MIP-2增加的意义尚不清楚。
