Hydrogen sulfide mimics hypoxic respiratory depression in the isolated brainstem of bullfrogs (Lithobates catesbeianus). (714.3)

Previous studies have shown that hypoxia causes a significant depression or cessation of fictive breathing in post‐metamorphic and adult bullfrog brainstems. We tested the hypothesis that hydrogen sulfide (H2S)contributes to the hypoxic‐induced inhibition of fictive breathing in the isolated bullfrog brainstem. Our hypothesis is based on findings that H2S contributes to hypoxia‐induced reflexes in vascular tissue and may be an important oxygen‐sensing signaling molecule. Brainstems from adult L. catesbeianus were placed in a recording chamber at room temperature (22 °C) and superfused continuously with an artificial CSF (aCSF) bubbled with 98% O2/2% CO2 (control), hypoxic aCSF (98% N2/2% CO2) or sodium sulfide (Na2S ∙ 9H2O ‐ a H2S donor) in control aCSF. Fictive breathing was recorded with suction electrodes applied to cranial nerves that normally innervate respiratory muscles. Brainstem hypoxia caused a significant reduction of fictive breathing from 10 ± 0.4 bursts/min (pre‐hypoxia) to 0.1 ± 0.1 bursts/min (hypoxia). Sodium sulfide (100 μM) caused a similar reduction of fictive lung bursts from 9.3 ± 7.2 bursts/min (pre H2S) to 0.1 ± 0.1 bursts/min (H2S). The results indicate that hypoxia inhibits fictive breathing in the isolated L. catesbeianus brainstem, and that H2S mimics the response to hypoxia. Hydrogen sulfide may be a key molecule for the hypoxia‐induced respiratory depression in the amphibian brainstem.