Oxygen pretreatment as protection against decompression sickness in rats: pressure and time necessary for hypothesized denucleation and renucleation

Abstract

Pretreatment with HBO at 300-500 kPa for 20 min reduced the incidence of decompression sickness (DCS) in a rat model. We investigated whether this procedure would be effective with lower oxygen pressures and shorter exposure, and tried to determine how long the pretreatment would remain effective. Rats were pretreated with oxygen at 101 or 203 kPa for 20 min and 304 kPa for 5 or 10 min. After pretreatment, the animals were exposed to air at 1,013 kPa for 33 min followed by fast decompression. Pretreatment at 101 or 203 kPa for 20 min and 304 kPa for 10 min significantly reduced the number of rats with DCS to 45%, compared with 65% in the control group. However, after pretreatment at 304 kPa for 5 min, 65% of rats suffered DCS. When pretreatment at 304 kPa for 20 min was followed by 2 h in normobaric air before compression and decompression, the outcome was worse, with 70-90% of the animals suffering DCS. This is probably due to the activation of "dormant" micronuclei. The risk of DCS remained lower (43%) when pretreatment with 100% O(2) at normobaric pressure for 20 min was followed by a 2 h interval in normobaric air (but not 6 or 24 h) before the hyperbaric exposure. The loss of effectiveness after a 6 or 24 h interval in normobaric air is related to micronuclei rejuvenation. Although pretreatment with hyperbaric O(2) may have an advantage over normobaric hyperoxia, decompression should not intervene between pretreatment and the dive.

Heat-shock protein 70 is involved in hyperbaric oxygen preconditioning on decompression sickness in rats

“…HBO before diving could replace the resident gas in the micronuclei by oxygen, which could be consumed by mitochondria and thus resulted in a reduced volume and number of micronuclei. 24 Furthermore, HBO increased NO production, 8,25 and NO may influence the degree of DCS bubble formation. 26,27 In the tissues well supplied of blood, microbubbles flow from capillary vessels into veins, circulate to the right heart and sequestered in the lung through pulmonary vasculature.…”

Oxygen breathing or recompression during decompression from nitrox dives with a rebreather: effects on intravascular bubble burden and ramifications for decompression profiles

“…Pure oxygen breathing increases the arterial oxygen partial pressure (O 2 pp) and causes the inert gas partial pressure to drop, reducing the degree of supersaturation and bubble formation from gas nuclei (Hamilton and Thalmann 2003;Arieli et al 2011). On the other hand, the predictions of the tissue bubble dynamics model suggest that an intermittent recompression (pressure effect) during the course of decompression could be another effective method for controlling the gas phase growth and decompression stress (Gernhardt 1991).…”

A New Measure of Decompression Sickness in the Rat

“…In one study a weighted severity score was given according to the number of animals and perceived “severity” of the signs [34]. Objective measures have been proposed such as a walking assessment in a rotating cylindrical cage [18, 25, 33, 35, 36], bubble grades [27, 37, 38], platelet counts [27], nitric oxide [39], bronchoalveolar and/or pleural fluids [39], inflammatory mediators (thromboxane B 2 and leukotriene E 4 ) [39], interleukin-6 [30], whole blood and differential cell counts [39], neutrophils [39], EGR-1/ B -actin ratio in the lung [20], time to lose equilibrium following ether anesthesia [40], lactic dehydrogenase (LDH), and creatine phosphokinase (CPK) plasma activity [29]. Only rarely have objective measures been correlated with subjective observer agreement.…”