Effect of inhaled hydrogen sulfide on metabolic responses in anesthetized, paralyzed, and mechanically ventilated piglets*

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.

[1]  T. Su,et al.  Further studies on opioids and hibernation: delta opioid receptor ligand selectively induced hibernation in summer-active ground squirrels. , 1988, Life sciences.

[2]  D. Keilin,et al.  Cytochrome a and Cytochrome Oxidase , 1938, Nature.

[3]  A. Redington,et al.  Oxygen consumption after cardiopulmonary bypass surgery in children: determinants and implications. , 2000, The Journal of thoracic and cardiovascular surgery.

[4]  M. Roth,et al.  Carbon monoxide-induced suspended animation protects against hypoxic damage in Caenorhabditis elegans , 2004, Proceedings of the National Academy of Sciences of the United States of America.

[5]  C. Thiemermann,et al.  THE PRODUCTION OF HYDROGEN SULFIDE LIMITS MYOCARDIAL ISCHEMIA AND REPERFUSION INJURY AND CONTRIBUTES TO THE CARDIOPROTECTIVE EFFECTS OF PRECONDITIONING WITH ENDOTOXIN, BUT NOT ISCHEMIA IN THE RAT , 2006, Shock.

[6]  D. Dorman,et al.  Olfactory Mucosal Necrosis in Male CD Rats Following Acute Inhalation Exposure to Hydrogen Sulfide: Reversibility and the Possible Role of Regional Metabolism , 2002, Toxicologic pathology.

[7]  J. Monro,et al.  Induced hypothermia in the management of refractory low cardiac output states following cardiac surgery in infants and children. , 1992, European journal of cardio-thoracic surgery : official journal of the European Association for Cardio-thoracic Surgery.

[8]  D. Dorman,et al.  Respiratory tract toxicity of inhaled hydrogen sulfide in Fischer-344 rats, Sprague-Dawley rats, and B6C3F1 mice following subchronic (90-day) exposure. , 2004, Toxicology and applied pharmacology.

[9]  M. Roth,et al.  H2S Induces a Suspended Animation–Like State in Mice , 2005, Science.

[10]  D. Sessler Complications and Treatment of Mild Hypothermia , 2001, Anesthesiology.

[11]  P. Moore,et al.  Role of hydrogen sulfide in cecal ligation and puncture-induced sepsis in the mouse. , 2006, American journal of physiology. Lung cellular and molecular physiology.