Journal of Applied Physiology
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J Appl Physiol (July 19, 2002). doi:10.1152/japplphysiol.00349.2002
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Articles in PresS, published online ahead of print July 19, 2002
J Appl Physiol, 10.1152/jap.00349.2002
Submitted on April 18, 2002
Accepted on July 2, 2002

Modulation of decompression sickness risk in pigs with caffeine during H2 biochemical decompression

Andreas Fahlman1, Winston C. Lin2, William B. Whitman2, and Susan R. Kayar1*

1 Environmental Physiology Department, Naval Medical Research Center, Silver Spring, Maryland, USA
2 Microbiology Department, University of Georgia, Athens, Georgia, USA

* To whom correspondence should be addressed. E-mail: kayars{at}ncrr.nih.gov.

In H2 biochemical decompression, H2-metabolizing intestinal microbes remove gas stored in tissues of animals breathing hyperbaric H2, thereby reducing decompression sickness (DCS) risk. We hypothesized that increasing intestinal perfusion in pigs would increase the activity of intestinal Methanobrevibacter smithii, lowering DCS incidence further. Pigs (Sus scrofa, 17-23 kg, n = 20) that ingested caffeine (5 mg . kg-1) increased O2 consumption rate in 1 atm air by ~20% for at least 3 h. Pigs were given caffeine alone(CA+INJ-) or caffeine plus injections of M. smithii (CA+INJ+). Animals were compressed to 24 atm (20.5-23.1 atm H2, 0.3-0.5 atm O2) for 3 h, then decompressed and observed for signs of DCS. In previous studies, DCS incidence in animals without caffeine treatment was significantly (P < 0.05) lower with M. smithii injections (CA-INJ+; 7/16) than in controls (CA-INJ-; 9/10). Contrary to our hypothesis, DCS incidence was marginally higher (P = 0.057) in CA+INJ+ (9/10) than in CA+INJ- (4/10). More information on tissue gas kinetics is needed before extending H2 biochemical decompression to humans.






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