Impact of body temperature on cardiovascular responses during hydrogen sulfide (H 2 S) breathing

Induction of a reversible “suspended animation” state by H 2 S breathing may preserve organ function in very ill patients. In this study, we measured the cardiovascular and metabolic effects of breathing H 2 S in mice. In C57BL6 mice with telemeters, breathing H 2 S (80 ppm) at 27°C ambient temperature (T a ) for 6 h, markedly reduced heart rate (HR) (520±20 to 258±34bpm, mean±SE, P<0.05), core body temperature (T b ) (from 37.3±0.4 to 29.2±0.5, P<0.05), activity and respiratory rate (RR), but not mean arterial pressure (MAP). Values returned to control after breathing air for 3 h. Echocardiography demonstrated H 2 S reduced HR (from 690±19 to 233±23 bpm, P<0.05) and cardiac output (CO, from 19±1 to 7±1 ml/min P<0.05) but preserved stroke volume (SV). To determine if the inhibitory effects of H 2 S on metabolism were due to hypothermia, we studied the response to breathing H 2 S in a warm chamber. Inhaling H 2 S for 6h with T b of 35°C decreased HR, activity, RR and CO (from 19±1 to 10±1 ml/min P<0.05), preserved SV, and increased MAP compared to 27°C H 2 S breathing (P<0.05). Exhaled CO 2 production was measured in mice breathing H 2 S for 30 min at either 27 or 35°C. Breathing H 2 S for 5 min decreased CO 2 production in both groups (from 50±6 to 28±2 and from 59±1 to 44±1 μM/min respectively, both P<0.05 vs. baseline). These results suggest breathing 80ppm H 2 S reversibly decreases murine metabolic rate. Supported by NIH grants HL 42397and 71987.