TY - JOUR
T1 - Oxygen-related chemoreceptor drive to breathe during H2S infusion
AU - Haouzi, Philippe
AU - Sonobe, Takashi
AU - Chenuel, Bruno
N1 - Funding Information:
This work has been supported in part by the Counter ACT Program, National Institutes of Health Office of the Director (NIH OD), and the National Institute of Neurological Disorders and Stroke (NINDS), Grant no. 1R21NS080788-01 . Takashi Sonobe isa researcher in the Department of Cardiac Physiology, National Cerebral and Cardio-vascular Center, Osaka, Japan, and is currently supported by a “Grant-in-Aid” for scientific research (N11J10987) from the Ministry of Education, Culture, Sports, Science and Technology of Japan.
PY - 2014/9/15
Y1 - 2014/9/15
N2 - This study addresses the following question: Could the acute depression in breathing produced by hyperoxia, a reflection of the tonic drive to breathe from the arterial chemoreceptors, be accounted for by a background level of endogenous H2S? To address this question, we produced a stable but moderate increase in breathing (24±11%) via continuous infusion of low levels of H2S, in 10 spontaneously breathing urethane-sedated rats. We found that acute exposure to 100% O2 (20 tests) decreased minute ventilation (V̇I) from 301±51 to 210±43ml/min within 15s in control conditions, but no additional significant drop in V̇I was observed during H2S induced hyperpnea. In addition, no decrease in the estimated concentrations of gaseous H2S in the arterial blood was observed during the hyperoxic tests. It is concluded that the ventilatory depression induced by high O2 appears to be limited to the tonic background peripheral chemosensory drive to breathe, but has little or no impact on the CB stimulation produced by low levels of H2S.
AB - This study addresses the following question: Could the acute depression in breathing produced by hyperoxia, a reflection of the tonic drive to breathe from the arterial chemoreceptors, be accounted for by a background level of endogenous H2S? To address this question, we produced a stable but moderate increase in breathing (24±11%) via continuous infusion of low levels of H2S, in 10 spontaneously breathing urethane-sedated rats. We found that acute exposure to 100% O2 (20 tests) decreased minute ventilation (V̇I) from 301±51 to 210±43ml/min within 15s in control conditions, but no additional significant drop in V̇I was observed during H2S induced hyperpnea. In addition, no decrease in the estimated concentrations of gaseous H2S in the arterial blood was observed during the hyperoxic tests. It is concluded that the ventilatory depression induced by high O2 appears to be limited to the tonic background peripheral chemosensory drive to breathe, but has little or no impact on the CB stimulation produced by low levels of H2S.
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U2 - 10.1016/j.resp.2014.05.012
DO - 10.1016/j.resp.2014.05.012
M3 - Article
C2 - 24973475
AN - SCOPUS:84904755338
SN - 1569-9048
VL - 201
SP - 24
EP - 30
JO - Respiratory Physiology and Neurobiology
JF - Respiratory Physiology and Neurobiology
ER -