Acclimation to decompression sickness in rats
Naval Medical Research Center, 503 Robert Grant Ave., Silver Spring, MD 20910-7800, USA.Journal of Applied Physiology (Impact Factor: 3.06). 03/2010; 108(3):596-603. DOI: 10.1152/japplphysiol.00596.2009
Protection against decompression sickness (DCS) by acclimation to hyperbaric decompression has been hypothesized but never proven. We exposed rats to acclimation dives followed by a stressful "test" dive to determine whether acclimation occurred. Experiments were divided into two phases. Phase 1 rats were exposed to daily acclimation dives of hyperbaric air for 30 min followed by rapid decompression on one of the following regimens: 70 ft of seawater (fsw) for 9 days (L70), 70 fsw for 4 days (S70), 40 fsw for 9 days (L40), 40 fsw for 4 days (S40), or unpressurized sham exposure for 9 days (Control). On the day following the last exposure, all were subjected to a "test" dive (175 fsw, 60 min, rapid decompression). Both L70 and S70 rats had significantly lower incidences of DCS than Control rats (36% and 41% vs. 62%, respectively). DCS incidences for the other regimens were lower than in Control rats but without statistical significance. Phase 2 used the most protective regimen from phase 1 (L70); rats were exposed to L70 or a similar regimen with a less stressful staged decompression. Another group was exposed to a single acclimation dive (70 fsw/30 min) on the day before the test dive. We observed a nonsignificant trend for the rapidly decompressed L70 dives to be more protective than staged decompression dives (44% vs. 51% DCS incidence). The single acclimation dive regimen did not provide protection. We conclude that protection against DCS can be attained with acclimating exposures that do not themselves cause DCS. The deeper acclimation dive regimens (70 fsw) provided the most protection.
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ABSTRACT: Previous studies demonstrated that animals exposed to repeated compression-decompression stress acclimated (i.e., developed reduced susceptibility) to rapid decompression. This study endeavored to characterize inflammatory and stress-related gene expression and signal transduction associated with acclimation to rapid decompression. Rats were divided into four groups: 1) control-sham: pressure naïve rats; 2) acclimation-sham: nine acclimation dives [70 feet seawater (fsw), 30 min]; 3) control-dive: test dive only (175 fsw, 60 min); and 4) acclimation-dive: nine acclimation dives and a test dive. After the test dive, rats were observed for decompression sickness (DCS). Expression of 13 inflammatory and stress-related genes and Akt (or PKB, a serine/threonine protein kinase) and MAPK phosphorylation of lung tissue were examined. The expression of immediate early gene/transcription factor early growth response gene 1 (Egr-1) was observed in both control and acclimation animals with DCS but not in animals without DCS. Increased Egr-1 in control-dive animals with DCS was significantly greater than in acclimation-dive animals with DCS. TNF-α, IL-1β, IL-6, and IL-10 were significantly elevated in control-DCS animals. Acclimation-DCS animals had increased TNF-α, but there was no change in IL-1β, IL-6, and IL-10. High levels of Akt phosphorylation were observed in lungs of acclimation-sham, acclimation-dive, and control-dive animals; phosphorylated ERK1/2 was only observed in animals with DCS. This study suggests that activation of ERK1/2 and upregulation of Egr-1 and its target cytokine genes by rapid decompression may play a role in the initiation and progression of DCS. It may be that the downregulated expression of these genes in animals with DCS is associated with previous exposure to repeated compression-decompression cycles. This study represents an initial step toward understanding the molecular mechanisms associated with acclimation to decompression.
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ABSTRACT: Acclimatization (an adaptive change in response to repeated environmental exposure) to diving could reduce decompression stress. A decrease in post-dive circulating venous gas emboli (VGE or bubbles) would represent positive acclimatization. The purpose of this study was to determine whether four days of daily diving alter post-dive bubble grades. 16 male divers performed identical no-decompression air dives on 4 consecutive days to 18 meters of sea water for 47 min bottom times. VGE monitoring was performed with transthoracic echocardiography every 20 min for 120 min post-dive. Completion of identical daily dives resulted in progressively decreasing odds (or logit risk) of having relatively higher grade bubbles on consecutive days. The odds on Day 4 were half that of Day 1 (OR 0.50, 95% CI: 0.34, 0.73). The odds ratio for a >III bubble grade on Day 4 was 0.37 (95% CI: 0.20, 0.70) when compared to Day 1. The current study indicates that repetitive daily diving may reduce bubble formation, representing a positive (protective) acclimatization to diving. Further work is required to evaluate the impact of additional days of diving and multiple dive days and to determine if the effect is sufficient to alter the absolute risk of decompression sickness.
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ABSTRACT: During scuba diving, the circulatory system is stressed by an elevated partial pressure of oxygen while the diver is submerged and by decompression-induced gas bubbles on ascent to the surface. This diving-induced stress may trigger decompression illness, but the majority of dives are asymptomatic. In this study we have mapped divers' blood transcriptomes with the aim of identifying genes, biological pathways and cell types perturbed by the physiological stress in asymptomatic scuba diving. Ten experienced divers abstained from diving for more than two weeks before performing a three-day series of daily dives to 18 meters depth for 47 minutes while breathing compressed air. Blood for microarray analysis was collected before and immediately after the first and last dives, and ten matched non-divers provided controls for pre-dive stationary transcriptomes. MetaCore GeneGo analysis of the pre-dive samples identified stationary upregulation of genes associated with apoptosis, inflammation and innate immune responses in the divers, most significantly involving genes in the TNFR1 pathway of caspase-dependent apoptosis, HSP60/HSP70 signaling via TLR4 and NF-κB-mediated transcription. Diving caused pronounced shifts in transcription patterns characteristic of specific leukocytes, with downregulation of genes expressed by CD8+ T lymphocytes and NK cells and upregulation of genes expressed by neutrophils, monocytes and macrophages. Antioxidant genes were upregulated. Similar transient responses were observed after the first and last dive. The results indicate that sub-lethal oxidative stress elicits the myeloid innate immune system in scuba diving, and that extensive diving may cause persistent change in pathways controlling apoptosis, inflammation and innate immune responses.
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