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Endogenous preoptic hydrogen sulphide attenuates hypoxia-induced hyperventilation.

M Kwiatkoski1, R N Soriano, G S F da Silva

  • 1Medical School of Ribeirão Preto, University of São Paulo, Ribeirão Preto, SP, Brazil.

Acta Physiologica (Oxford, England)
|October 15, 2013
PubMed
Summary

Hydrogen sulfide (H2S) in the anteroventral preoptic region (AVPO) inhibits the body's response to low oxygen. Increased H2S during hypoxia reduces ventilation, suggesting a metabolic link.

Keywords:
aminooxyacetatecystathionine beta-synthasehyperpneahypothalamussodium sulphideventilation

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Area of Science:

  • Neuroscience
  • Respiratory Physiology
  • Biochemistry

Background:

  • The anteroventral preoptic region (AVPO) integrates thermal and cardiorespiratory responses to hypoxia.
  • Hydrogen sulfide (H2S) synthesis increases in the AVPO under hypoxic conditions.

Purpose of the Study:

  • To investigate the role of H2S in the AVPO in modulating the hypoxic ventilatory response.

Main Methods:

  • Rats were administered intracerebroventricularly or intra-AVPO with an H2S synthesis inhibitor (aminooxyacetate) or an H2S donor (Na2S).
  • Pulmonary ventilation and deep body temperature were measured during hypoxia (7% O2).
  • AVPO H2S levels were assessed in rats exposed to hypoxia.

Main Results:

  • Hypoxia increased ventilation, an effect potentiated by the H2S synthesis inhibitor and attenuated by the H2S donor.
  • AVPO H2S production increased during hypoxia, correlating with reduced hyperventilation and lower body temperature.
  • The H2S synthesis inhibitor reduced hypoxia-induced H2S production, suggesting endogenous synthesis.

Conclusions:

  • AVPO H2S production is stimulated by hypoxia.
  • H2S acts as an inhibitory modulator of the hypoxic ventilatory response.
  • H2S modulation of hypoxia-induced hyperventilation is likely proportional to metabolism.