Heat stress attenuates air bubble-induced acute lung injury: a novel mechanism of diving acclimatization

Abstract

Diving acclimatization refers to a reduced susceptibility to acute decompression sickness (DCS) in individuals undergoing repeated compression-decompression cycles. We postulated that mechanisms responsible for the acclimatization are similar to that of a stress preconditioning. In this study, we investigated the protective effect of prior heat shock treatment on air embolism-induced lung injury and on the incidence of DCS in rats. We exposed rats (n = 31) to a pressure cycle that induced signs of severe DCS in 48% of the rats, greater wet-to-dry ratio (W/D) of lung weight compared with the control group (5.48 +/- 0.69 vs. 4.70 +/- 0.17), and higher protein concentration in bronchoalveolar lavage (BAL) fluid (362 +/- 184 vs. 209 +/- 78 mg/l) compared with the control group. Rats with DCS expressed more heat shock protein 70 (HSP70) in the lungs than those without signs of disease. Prior heat shock (n = 12) increased the expression of HSP70 in the lung and attenuated the elevation of W/D of lung weight (5.03 +/- 0.17) after the identical decompression protocol. Prior heat shock reduced the incidence of severe DCS by 23%, but this failed to reach statistical significant (chi(2) = 1.94, P = 0.163). Venous air infusion (1.0 ml/40 min) caused profound hypoxemia (54.5 +/- 3.8 vs. 83.8 +/- 3.2 Torr at baseline; n = 6), greater W/D of lung weight (5.98 +/- 0.45), and high protein concentration in BAL fluid (595 +/- 129 mg/l). Prior heat shock (n = 6) did not alter the level of hypoxemia caused by air embolism, but it accelerated the recovery to normoxemia after air infusion was stopped. Prior heat shock also attenuated the elevation of W/D of lung weight (5.19 +/- 0.40) and the increase in BAL protein (371 +/- 69 mg/l) in air embolism group. Our results showed that the occurrence of DCS after rapid decompression is associated with increased expression of a stress protein (HSP70) and that prior heat shock exposure attenuates the air bubble-induced lung injury. These results suggest that bubble formation in tissues activates a stress response and that stress preconditioning attenuates lung injury on subsequent stress, which may be the mechanism responsible for diving acclimatization.

Pre-Dive Vibration Effect on Bubble Formation After a 30-m Dive Requiring a Decompression Stop

“…The role of heat shock proteins as a primary mediator of diving acclimatization has been investigated ( 17 ). For this study, we hypothesized that gas nuclei may also be depleted by mechanical means, rather than biochemical means.…”

Simulated diving after heat stress potentiates the induction of heat shock protein 70 and elevates glutathione in human endothelial cells

“…Similar results have previously been demonstrated in rats that were subjected to rapid decompression. Occurrence of DCS was associated with increased HSP70 expression and heat shock prior to diving reduced air bubble-induced lung injury (Huang et al 2003). Recent experiments with rats exposed to rapid decompression indicated an association between occurrence of DCS and increased gene expression of small heat shock proteins in brain and lung, but not in liver.…”

Gas embolization of the liver in a rat model of rapid decompression

“…However, the possibility that gas embolism may indirectly induce cellular damage by activating plasma factors of inflammatory response (such as cytokines, TNF-␣, etc.) (10,14,18), as well as a systemic stress response, should also be considered. As a matter of fact, the evidence of centrilobular necrosis at 24 h in two cases of repeated rapid decompression (protocol B) strongly suggests that repeated hepatic injury by gas embolism can lead to cellular death and fibrosis.…”