Heat shock stress prior to hyperbaric oxygen exposure in rats

Heat shock proteins (HSPs) and nuclear factor-kappa B (NF-kappaB) have been established as important mediators in lung injury; however, their role in preventing pulmonary toxicity from hyperbaric oxygen (HBO) has not been evaluated.

We aimed to study the effects of heat shock (HS) injury on hyperbaric hyperoxic lung injury (HHLI) in a rat model and identify a mechanism of protection by evaluating HSP 27 and HSP 70 mRNA and protein levels, NF-kappaB p65, lung injury and oxidative parameters. By varying the times between HS and exposure to HBO, the pathways of interaction between HSPs and NF-kappaB will be further clarified.

Our results showed that HS exposure increases the mRNA and protein levels of HSP 27 and HSP 70; HS induced 10-fold increases of HSP 27 (9.77 +/- 0.60) and HSP 70 (10.33 +/- 2.4) within the first 10 h compared to control animals. Lesion scores were higher for the first 16 h after HS, but decreased again after 31 h (N = 7 animals; 5 lesions scores). Protein nitration showed no significant differences between groups exposed to HS or HBO; similarly there was no difference with a combination of both treatments.

HBO appears to attenuate the HS response by HSP 27 and HSP 70. Histopathology results suggest that HS might mitigate pathology in animals exposed to HS and HBO. No significant effect of HS on HBO-induced HHLI was observed in animals treated with both HS and HBO.