Cardiac and metabolic effects of hypothermia and inhaled hydrogen sulfide in anesthetized and ventilated mice

Katja Baumgart, Florian Wagner, Michael Gröger, Sandra Weber, Eberhard Barth, Josef A. Vogt, Ulrich Wachter, Markus Huber-Lang, Markus W. Knöferl, Gerd Albuszies, Michael Georgieff, Pierre Asfar, Csaba Szabo, Enrico Calzia, Peter Radermacher, Vladislava Simkova

Research output: Contribution to journalArticle

37 Citations (Scopus)

Abstract

Objective: To test the hypothesis whether inhaled hydrogen sulfide amplifies the effects of deliberate hypothermia during anesthesia and mechanical ventilation as hypothermia is used to provide organ protection after brain trauma or circulatory arrest. Awake mice inhaling hydrogen sulfide exhibit reduced energy expenditure, hypothermia, and bradycardia despite unchanged systolic heart function. In rodents, anesthesia alone causes decreased metabolic rate and thus hypothermia and bradycardia. Design: Prospective, controlled, randomized study. Setting: University animal research laboratory. Subjects: Male C57/B6 mice. Interventions: After surgical instrumentation (central venous, left ventricular pressure-conductance catheters, ultrasound flow probes on the portal vein and superior mesenteric artery), normo-or hypothermic animals (core temperature = 38°C and 27°C) received either 100 ppm hydrogen sulfide or vehicle over 5 hrs (3 hrs hydrogen sulfide during normothermia). Measurements and Main Results: During normothermia, hydrogen sulfide had no hemodynamic or metabolic effect. With or without hydrogen sulfide, hypothermia decreased blood pressure, heart rate, and cardiac output, whereas stroke volume, ejection fraction, and end-diastolic pressure remained unaffected. Myocardial and hepatic oxidative deoxyribonucleic acid damage (comet assay) and endogenous glucose production (rate of appearance of 1,2,3,4,5,6-C6-glucose) were similar in all groups. Hypothermia comparably decreased CO2 production with or without inhaled hydrogen sulfide. During hypothermia, inhaled hydrogen sulfide increased the glucose oxidation rate (derived from the expiratory CO2/CO2 ratio). This shift toward preferential carbohydrate utilization coincided with a significantly attenuated responsiveness of hepatic mitochondrial respiration to stimulation with exogenous cytochrome-c-oxidase (high-resolution respirometry). Conclusions: In anesthetized and mechanically ventilated mice, inhaled hydrogen sulfide did not amplify the systemic hemodynamic and cardiac effects of hypothermia alone. The increased aerobic glucose oxidation together with the reduced responsiveness of cellular respiration to exogenous cytochrome-c stimulation suggest that, during hypothermia, inhaled hydrogen sulfide improved the yield of mitochondrial respiration, possibly via the maintenance of mitochondrial integrity. Hence, inhaled hydrogen sulfide may offer metabolic benefit during therapeutic hypothermia.

Original languageEnglish (US)
Pages (from-to)588-595
Number of pages8
JournalCritical Care Medicine
Volume38
Issue number2
DOIs
StatePublished - Feb 2010

Fingerprint

Hydrogen Sulfide
Hypothermia
Glucose
Bradycardia
Respiration
Anesthesia
Hemodynamics
Cell Respiration
Blood Pressure
Induced Hypothermia
Comet Assay
Superior Mesenteric Artery
Liver
Ventricular Pressure
Electron Transport Complex IV
Portal Vein
Cytochromes c
Artificial Respiration
Cardiac Output
Stroke Volume

Keywords

  • Comet assay
  • Cytochrome-c-oxidase
  • Glucose oxidation
  • Glucose production
  • Mitochondrial respiration
  • Pressure-conductance catheter
  • Suspended animation

ASJC Scopus subject areas

  • Critical Care and Intensive Care Medicine

Cite this

Baumgart, K., Wagner, F., Gröger, M., Weber, S., Barth, E., Vogt, J. A., ... Simkova, V. (2010). Cardiac and metabolic effects of hypothermia and inhaled hydrogen sulfide in anesthetized and ventilated mice. Critical Care Medicine, 38(2), 588-595. https://doi.org/10.1097/CCM.0b013e3181b9ed2e

Cardiac and metabolic effects of hypothermia and inhaled hydrogen sulfide in anesthetized and ventilated mice. / Baumgart, Katja; Wagner, Florian; Gröger, Michael; Weber, Sandra; Barth, Eberhard; Vogt, Josef A.; Wachter, Ulrich; Huber-Lang, Markus; Knöferl, Markus W.; Albuszies, Gerd; Georgieff, Michael; Asfar, Pierre; Szabo, Csaba; Calzia, Enrico; Radermacher, Peter; Simkova, Vladislava.

In: Critical Care Medicine, Vol. 38, No. 2, 02.2010, p. 588-595.

Research output: Contribution to journalArticle

Baumgart, K, Wagner, F, Gröger, M, Weber, S, Barth, E, Vogt, JA, Wachter, U, Huber-Lang, M, Knöferl, MW, Albuszies, G, Georgieff, M, Asfar, P, Szabo, C, Calzia, E, Radermacher, P & Simkova, V 2010, 'Cardiac and metabolic effects of hypothermia and inhaled hydrogen sulfide in anesthetized and ventilated mice', Critical Care Medicine, vol. 38, no. 2, pp. 588-595. https://doi.org/10.1097/CCM.0b013e3181b9ed2e
Baumgart, Katja ; Wagner, Florian ; Gröger, Michael ; Weber, Sandra ; Barth, Eberhard ; Vogt, Josef A. ; Wachter, Ulrich ; Huber-Lang, Markus ; Knöferl, Markus W. ; Albuszies, Gerd ; Georgieff, Michael ; Asfar, Pierre ; Szabo, Csaba ; Calzia, Enrico ; Radermacher, Peter ; Simkova, Vladislava. / Cardiac and metabolic effects of hypothermia and inhaled hydrogen sulfide in anesthetized and ventilated mice. In: Critical Care Medicine. 2010 ; Vol. 38, No. 2. pp. 588-595.
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AU - Vogt, Josef A.

AU - Wachter, Ulrich

AU - Huber-Lang, Markus

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AU - Georgieff, Michael

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N2 - Objective: To test the hypothesis whether inhaled hydrogen sulfide amplifies the effects of deliberate hypothermia during anesthesia and mechanical ventilation as hypothermia is used to provide organ protection after brain trauma or circulatory arrest. Awake mice inhaling hydrogen sulfide exhibit reduced energy expenditure, hypothermia, and bradycardia despite unchanged systolic heart function. In rodents, anesthesia alone causes decreased metabolic rate and thus hypothermia and bradycardia. Design: Prospective, controlled, randomized study. Setting: University animal research laboratory. Subjects: Male C57/B6 mice. Interventions: After surgical instrumentation (central venous, left ventricular pressure-conductance catheters, ultrasound flow probes on the portal vein and superior mesenteric artery), normo-or hypothermic animals (core temperature = 38°C and 27°C) received either 100 ppm hydrogen sulfide or vehicle over 5 hrs (3 hrs hydrogen sulfide during normothermia). Measurements and Main Results: During normothermia, hydrogen sulfide had no hemodynamic or metabolic effect. With or without hydrogen sulfide, hypothermia decreased blood pressure, heart rate, and cardiac output, whereas stroke volume, ejection fraction, and end-diastolic pressure remained unaffected. Myocardial and hepatic oxidative deoxyribonucleic acid damage (comet assay) and endogenous glucose production (rate of appearance of 1,2,3,4,5,6-C6-glucose) were similar in all groups. Hypothermia comparably decreased CO2 production with or without inhaled hydrogen sulfide. During hypothermia, inhaled hydrogen sulfide increased the glucose oxidation rate (derived from the expiratory CO2/CO2 ratio). This shift toward preferential carbohydrate utilization coincided with a significantly attenuated responsiveness of hepatic mitochondrial respiration to stimulation with exogenous cytochrome-c-oxidase (high-resolution respirometry). Conclusions: In anesthetized and mechanically ventilated mice, inhaled hydrogen sulfide did not amplify the systemic hemodynamic and cardiac effects of hypothermia alone. The increased aerobic glucose oxidation together with the reduced responsiveness of cellular respiration to exogenous cytochrome-c stimulation suggest that, during hypothermia, inhaled hydrogen sulfide improved the yield of mitochondrial respiration, possibly via the maintenance of mitochondrial integrity. Hence, inhaled hydrogen sulfide may offer metabolic benefit during therapeutic hypothermia.

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