Document Detail

Inflammatory Effects of Hypothermia and Inhaled H2S During Resuscitated, Hyperdynamic Murine Septic Shock.
MedLine Citation:
PMID:  20938376     Owner:  NLM     Status:  In-Data-Review    
Inhaling hydrogen sulfide (H2S) reduced energy expenditure resulting in hypothermia. Because the inflammatory effects of either hypothermia alone or H2S per se still are a matter of debate, we tested the hypothesis whether inhaled H2S amplifies the hypothermia-related modulation of the inflammatory response. Fifteen hours after cecal ligation and puncture or sham laparotomy, anesthetized and mechanically ventilated normothermic and hypothermic mice (core temperature kept at 38°C and 27°C, respectively) received either 100 ppm H2S or vehicle. In the sham-operated animals, inhaled H2S and hypothermia alone comparably reduced the plasma chemokine and IL-6 levels, but combining hypothermia and inhaled H2S had no additional effect. The lung tissue cytokine and chemokine patterns revealed a similar response. During sepsis, inhaled H2S reduced the blood cytokine concentrations only, without effects on the plasma chemokine or the lung tissue levels. Again, inhaled H2S had no major additional effect during hypothermia. With or without sepsis, inhaled H2S and hypothermia alone comparably reduced the lung tissue heme oxygenase 1 expression, whereas inhaled H2S had no additional effect during hypothermia. Lung tissue nuclear transcription factor κB activation was reduced by combining H2S with hypothermia in the sham-operated animals, whereas it was increased by inhaled H2S during sepsis. Hypothermia amplified this response. Hence, during anesthesia and mechanical ventilation, inhaled H2S exerted anti-inflammatory effects, which were, however, not amplified by adding deliberate hypothermia. Sepsis attenuated these anti-inflammatory effects of inhaled H2S, which were at least in part independent of the nuclear transcription factor κB pathway.
Florian Wagner; Katja Wagner; Sandra Weber; Bettina Stahl; Markus W Knöferl; Markus Huber-Lang; Daniel H Seitz; Pierre Asfar; Enrico Calzia; Uwe Senftleben; Florian Gebhard; Michael Georgieff; Peter Radermacher; Vladislava Hysa
Related Documents :
19678906 - Cell death in sepsis: a matter of how, when, and where.
11197596 - Immune balance in critically ill patients.
20714106 - New players in the sepsis-protective activated protein c pathway.
25482676 - Dilong prevents the high- kcl cardioplegic solution administration-induced apoptosis in...
23092856 - Kinetic analysis and evaluation of the mechanisms involved in the resolution of experim...
16950286 - Prenatal initiation of endotoxin airway exposure prevents subsequent allergen-induced s...
Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Shock (Augusta, Ga.)     Volume:  35     ISSN:  1540-0514     ISO Abbreviation:  Shock     Publication Date:  2011 Apr 
Date Detail:
Created Date:  2011-03-16     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  9421564     Medline TA:  Shock     Country:  United States    
Other Details:
Languages:  eng     Pagination:  396-402     Citation Subset:  IM    
*Sektion Anästhesiologische Pathophysiologie und Verfahrensentwicklung, Klinik für Anästhesiologie, and †Klinik für Unfall-, Hand-, Plastische und Wiederherstellungschirurgie, Universitätsklinikum Ulm, Germany; and ‡Laboratoire HIFIH, UPRES EA 3859, IFR 132, Université d'Angers, Département de Réanimation Médicale et de Médecine Hyperbare, Centre Hospitalo-Universitaire, Angers, France.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  Prevalence of Chlamydia trachomatis and Neisseria gonorrhoeae and repeat infection among pregnant ur...
Next Document:  Improved renal recovery with postresuscitation N-acetylcysteine treatment in asphyxiated newborn pig...