Objective: Induced hypometabolism may improve the balance between oxygen delivery and consumption and may help sustain tissue viability in critically ill patients with low cardiac output state. Inhaled hydrogen sulfide (H2S) has been shown to induce a suspended animation-like state in mice with a 90% decrease in oxygen consumption. We conducted a preclinical study to explore the potential effect of H2S on metabolic rate in large mammals.
Design: Prospective study.
Setting: Animal laboratory in a university hospital.
Subjects: Eleven anesthetized, paralyzed, and mechanical ventilated piglets (5.8 ± 0.7 kg).
Interventions: The right carotid artery and superior vena cava were cannulated for arterial pressure monitoring and blood gas sampling. Seven piglets were sequentially exposed to 20, 40, 60, and 80 ppm of H2S over a period of 6 hrs (each level for 1.5 hrs) (H2S group), and additionally four piglets were exposed to air over the same period (control group).
Measurements and Main Results: Ambient temperature was fixed at 22°C throughout. Central body temperature, arterial pressure, and heart rate were continuously monitored. Oxygen consumption and carbon dioxide production were continuously measured using respiratory mass spectrometry. Cardiac output was calculated using the Fick principle. Central temperature and oxygen consumption significantly and linearly decreased over the H2S exposures (p < .0001 for both), the rates of which were significantly less compared with those in the control group (p < .01 for both). Mean arterial pressure increased significantly (p = .007), whereas heart rate (p = .14), cardiac output (p = .89), and lactate (p = .67) did not change significantly during H2S exposures in H2S group; all the variables decreased significantly in the control group (p < .01 for all), and p < .01 by comparison with H2S group except for lactate (p = .05).
Conclusions: H2S does not appear to have hypometabolic effects in ambiently cooled large mammals and conversely appears to act as a hemodynamic and metabolic stimulant.
From the Cardiac Program, Hospital for Sick Children, Toronto, Ontario, Canada (JL, GZ, AHR); and the Data Center, Congenital Heart Surgeons’ Society Database, Hospital for Sick Children, Toronto Ontario, Canada (SC).
*See also p. 129.
The authors have not disclosed any potential conflicts of interest.
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