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. 2023 Mar 6;192(2):247–264. doi: 10.1093/toxsci/kfad022

Figure 1.

Figure 1.

In vivo H2S-induced suppression of brain activity was concomitant with apnea. Mice were preimplanted with electrodes for EEG and EKG. Breathing activity was recorded by plethysmography. In vivo H2S exposure paradigm was shown in A. After brief calibration of plethysmograph and recordings of biopotentials of baseline activity, mice were exposed to normal breathing air or 1000 ppm H2S (B) until death as assesses by EKG. Baseline recordings displayed EEG, EKG, and plethysmography traces of mice at rest. Recording 1 shows 90 s signal recordings at about 5 min from the start of gas exposure, while Recording 2 shows 90 s signal recordings at about 35 min from the start of gas exposure. Recordings 1 and 2 display typical suppression of EEG and plethysmography in H2S exposed mice (B). Note the H2S-induced electrocerebral suppression and respiratory arrest while cardiac activity persisted (B, Recordings 1 and 2). N = 3 mice. Abbreviations: EEG, electroencephalogram; EKG, electrocardiogram; H2S, hydrogen sulfide.