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Effects of high peak airway pressure on the expression of heat shock protein 70 in rat lungs: a preliminary study
Author(s) -
Kira S.,
Mori M.,
Takatani J.,
Uchino T.,
Yasuda N.,
Miyakawa H.,
Noguchi T.
Publication year - 2006
Publication title -
acta anaesthesiologica scandinavica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.738
H-Index - 107
eISSN - 1399-6576
pISSN - 0001-5172
DOI - 10.1111/j.1399-6576.2005.00942.x
Subject(s) - hsp70 , medicine , ventilation (architecture) , lung , shock (circulatory) , mechanical ventilation , anesthesia , heat shock protein , airway , immunohistochemistry , pathology , andrology , biology , mechanical engineering , biochemistry , gene , engineering
Background: Heat shock protein 70 (HSP70) is induced by a wide variety of stresses in addition to hyperthermia. Recent studies have clarified that mechanical stretching and pressure overload can induce HSP70 in some tissues and cells. However, it remains unclear whether HSP70 is induced in stretch‐subjected lungs, such as those under mechanical ventilation. This study was designed to investigate the effects of high peak airway pressure (PAP) ventilation on HSP70 expression in intact rat lungs. Methods: Male Sprague‐Dawley rats were randomly allocated to one of three groups: non‐ventilated (anesthesia alone) control group; PAP 15 cmH 2 O group (P15); and PAP 30 cmH 2 O group (P30). The rats in the PAP groups were subjected to pressure‐controlled assisted ventilation at the appropriate PAP for 30 min. Rats were killed at 12, 24 and 48 h after ventilation or anesthesia alone, and the lungs were removed. The lung tissues were processed for immunohistochemical and Western blotting analyses of HSP70. Results: Following 30 min of pressure‐controlled assisted ventilation, HSP70 expression in the P30 group was significantly up‐regulated in bronchiolar cells and subepithelial tissues at 12 h, and this up‐regulation continued throughout the observation period. In contrast, there were no significant differences between the control and P15 groups, although the expression of HSP70 was higher in the P15 group than in the control group at all time points. Conclusions: HSP70 was induced by high PAP ventilation, but its specific role and induction mechanism remain unclear. Therefore, further investigations should be encouraged.