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DOES H2S TRANSDUCE THE EFFECTS OF HYPOXIA ON METABOLIC AND RESPIRATORY CONTROL IN MAMMALS?
Author(s) -
Haouzi Philippe A,
Bell Harold,
Ferguson Carrie,
Notet Veronique
Publication year - 2009
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.23.1_supplement.621.22
Subject(s) - hyperventilation , hypoxia (environmental) , respiratory system , respiration , metabolism , endocrinology , medicine , control of respiration , ventilation (architecture) , biology , chemistry , oxygen , anatomy , organic chemistry , mechanical engineering , engineering
Endogenous H2S appears to mediate some of the cardio‐vascular effects of hypoxia (H) in non mammalian species, while exposure to non toxic concentration of H2S reduces the metabolism in small mammals just like with H. Could H2S be an O2 sensor in mammals? We compared the ventilatory and metabolic effects of exposure to 60 ppm H2S and to 10 % O2 in small and large freely behaving rodents which responses to H differ according to body mass, i.e. 20 g mice and 500g rats. H2S and H produced a similar depression in metabolism in the mice (‐58 %), but not in the large rats. The relative hyperventilation produced by H in the mice (+23 %) was replaced by a ventilatory depression with H2S (‐53%) which paralleled the drop in metabolism. In the rats, ventilation was stimulated in H (+64%), but not with H2S. Adding H2S on top of H in the mice abolished the relative hyperventilation of H and provoked a much larger respiratory (and metabolic) depression. H2S does not mediate the effects of H on the arterial chemoreflex. The depressive effects of H2S and H on breathing, which is linked to the metabolic depression, is only expressed in small sized mammals and is compatible with the hypothesis.