Modulation of decompression sickness risk in pigs with caffeine during H2biochemical decompression
Author(s) -
Andreas Fahlman,
Winston Lin,
William B. Whitman,
Susan R. Kayar
Publication year - 2002
Publication title -
journal of applied physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.253
H-Index - 229
eISSN - 8750-7587
pISSN - 1522-1601
DOI - 10.1152/japplphysiol.00349.2002
Subject(s) - decompression sickness , caffeine , decompression , anesthesia , incidence (geometry) , biology , zoology , medicine , physiology , endocrinology , optics , physics
In H(2) biochemical decompression, H(2)-metabolizing intestinal microbes remove gas stored in tissues of animals breathing hyperbaric H(2), 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) increased O(2) consumption rate in 1 atm air by ~20% for at least 3 h. Pigs were given caffeine alone or caffeine plus injections of M. smithii. Animals were compressed to 24 atm (20.5-23.1 atm H(2), 0.3-0.5 atm O(2)) 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 (7/16) than in controls (9/10). However, contrary to our hypothesis, DCS incidence was marginally higher (P = 0.057) in animals that received caffeine and M. smithii (9/10) than in animals that received caffeine but no M. smithii (4/10). More information on gas kinetics is needed before extending H(2) biochemical decompression to humans.
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