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Endogenous preoptic hydrogen sulphide attenuates hypoxia‐induced hyperventilation
Author(s) -
Kwiatkoski M.,
Soriano R. N.,
da Silva G. S. F.,
Francescato H. D.,
Coimbra T. M.,
Glass M. L.,
Carnio E. C.,
Branco L. G. S.
Publication year - 2014
Publication title -
acta physiologica
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.591
H-Index - 116
eISSN - 1748-1716
pISSN - 1748-1708
DOI - 10.1111/apha.12177
Subject(s) - microinjection , hyperventilation , hypoxia (environmental) , chemistry , endocrinology , tidal volume , medicine , hypoxic ventilatory response , respiration , thermoregulation , oxygen , respiratory system , anatomy , organic chemistry
Aim We hypothesized that hydrogen sulphide ( H 2 S ), acting specifically in the anteroventral preoptic region ( AVPO – an important integrating site of thermal and cardiorespiratory responses to hypoxia in which H 2 S synthesis has been shown to be increased under hypoxic conditions), modulates the hypoxic ventilatory response. Methods To test this hypothesis, we measured pulmonary ventilation ( V ˙ E ) and deep body temperature of rats before and after intracerebroventricular (icv) or intra‐ AVPO microinjection of aminooxyacetate ( AOA ; CBS inhibitor) or N a 2 S ( H 2 S donor) followed by 60 min of hypoxia exposure (7% O 2 ). Furthermore, we assessed the AVPO levels of H 2 S of rats exposed to hypoxia. Control rats were kept under normoxia. Results Microinjection of vehicle, AOA or N a 2 S did not changeV ˙ E under normoxic conditions. Hypoxia caused an increase in ventilation, which was potentiated by microinjection of AOA because of a further augmented tidal volume. Conversely, treatment with N a 2 S significantly attenuated this response. The in vivo H 2 S data indicated that during hypoxia the lower the deep body temperature the smaller the degree of hyperventilation. Under hypoxia, H 2 S production was found to be increased in the AVPO , indicating that its production is responsive to hypoxia. The CBS inhibitor attenuated the hypoxia‐induced increase in the H 2 S synthesis, suggesting an endogenous synthesis of the gas. Conclusion These data provide solid evidence that AVPO H 2 S production is stimulated by hypoxia, and this gaseous messenger exerts an inhibitory modulation of the hypoxic ventilatory response. It is probable that the H 2 S modulation of hypoxia‐induced hyperventilation is at least in part in proportion to metabolism.