Abstract 2273: Cardiovascular Changes after Exposure to Hydrogen Sulfide in a Murine Model
Induction of a hibernation-like state may help to preserve organ function in critically-ill patients. Inhalation of hydrogen sulfide (H2S) has been shown to trigger a hibernation-like state in mice characterized by a reduction in activity and metabolism. However, the impact of H2S on the cardiovascular system is unknown. In this study, the effects of breathing H2S (80 parts per million) on the cardiovascular function were measured in C57BL6 mice implanted with telemetry devices measuring heart rate (HR) and blood pressure (BP) or temperature (T). Breathing H2S at an ambient T of 27°C decreased HR within 10 min reaching a plateau after 2 h (Table⇓).. Breathing H2S for 2 h decreased respiratory rate (RR) from 121±2.6 to 25±2.6 breaths per min (brpm, P<0.05). In contrast, breathing H2S for up to 6 h did not alter BP. Breathing H2S for 6 h decreased body core T from 38° to 30°C (n=4, P<0.05) associated with markedly decreased physical activity, although mice could move when provoked. Echocardiography confirmed that H2S breathing decreased HR (from 651±13 to 377±37, P<0.01) associated with a decrease in cardiac output from 11.3±1.1 to 2.8±1.5 ml/min, P< 0.01) but a preserved stroke volume (43±2 v/s 35±5 μl). All these changes were completely reversed after mice were returned to breathing air without H2S for 2 h. To evaluate the impact of ambient T on the cardiovascular response to H2S, mice were studied at an ambient T of 35°C. (Table 1⇓) Breathing H2S for 6 h at 35°C decreased HR (316±10 bpm, P<0.05) and respiratory rate (43±10 brpm, P<0.05) but to a lesser degree than breathing H2S at 27°C (P<0.05 for both), and blood pressure decreased to 117±0.6 mmHg (P<0.05). In conclusion, breathing H2S causes hypothermia, reduces RR, and decreases HR and cardiac output without significant changes in stroke volume or systemic blood pressure.