热预处理导致对脂多糖气管内滴注的炎症反应减弱。

Blunted inflammatory response to lipopolysaccharide endotracheal instillation due to thermal preconditioning.

作者信息

Di Filippo A, Rinaldi S, Pascente C, Messeri D, De Gaudio A R

机构信息

Section of Anaesthesia, Department of Critical Care, University of Florence, Viale Morgagni 85, 50124 Florence, Italy.

出版信息

Minerva Anestesiol. 2005 Oct;71(10):601-7.

PMID:16163150

Abstract

AIM

Heat shock proteins (HSPs), induced by thermal stress, make the cells more resistant to following stress. We aimed to verify if rats heating reduces the production of TNF-alpha in a model of acute respiratory distress syndrome (ARDS).

METHODS

We divided 34 Wistar rats in Group A and Group B. The rats of Group A received thermal shock and tracheal instillation of lipopolysaccharide (LPS), the rats of Group B only tracheal instillation of LPS. All the rats have been then subdivided in 6 subgroups sacrificed at different times after instillation of LPS: A30 and B30 at 30 min, A90 and B90 at 90 min and A180 and B180 at 180 min. We dosed the serum concentration of TNF-alpha and the values of every subgroup have been compared with the Student t-test.

RESULTS

The serum concentration of TNF-alpha in the subgroup A90 resulted significantly lower than in the subgroup B90.

CONCLUSIONS

The exposure to thermal stress resulting in the production of HSPs reduced the concentration of TNF-alpha in this model of ARDS.

摘要

目的

热应激诱导产生的热休克蛋白（HSPs）可使细胞对后续应激更具抵抗力。我们旨在验证在急性呼吸窘迫综合征（ARDS）模型中，对大鼠进行加热是否会降低肿瘤坏死因子-α（TNF-α）的产生。

方法

我们将34只Wistar大鼠分为A组和B组。A组大鼠接受热休克并气管内滴注脂多糖（LPS），B组大鼠仅气管内滴注LPS。然后，所有大鼠在滴注LPS后的不同时间被分为6个亚组并处死：滴注后30分钟的A30和B30、90分钟的A90和B90以及180分钟的A180和B180。我们测定了TNF-α的血清浓度，并使用学生t检验比较了每个亚组的值。