title: Inhaled hydrogen sulfide induces suspended animation, but does not alter the inflammatory response after blunt chest trauma.
abstract: The treatment of acute lung injury and septic complications after blunt chest trauma remains a challenge. Inhaled hydrogen sulfide (H₂S) may cause a hibernation-like metabolic state, which refers to an attenuated systemic inflammatory response. Therefore, we tested the hypothesis that inhaled H₂S-induced suspended animation may attenuate the inflammation after pulmonary contusion. Male Sprague-Dawley rats were subjected to blunt chest trauma (blast wave) or sham procedure and subsequently exposed to a continuous flow of H₂S (100 ppm) or control gas for 6 h. Body temperature and activity were measured by an implanted transmitter. At 6, 24, or 48 h after trauma, animals were killed, and the cellular contents of bronchoalveolar lavage (BAL) as well as cytokine concentrations in BAL, plasma, and culture supernatants of blood mononuclear cells, Kupffer cells, splenic macrophages, and splenocytes were determined. Hydrogen sulfide inhalation caused a significant reduction in body temperature and activity. The trauma-induced increase in alveolar macrophage counts was abrogated 48 h after trauma when animals received H₂S, whereas the trauma-induced increase in neutrophil counts was unaltered. Furthermore, H₂S inhalation partially attenuated the mediator release in BAL and culture supernatants of Kupffer cells as well as splenic cells; it altered plasma cytokine concentrations but did not affect the trauma-induced changes in mononuclear cell culture supernatants. These findings indicate that inhaled H₂S induced a reduced metabolic expenditure and partially attenuated inflammation after trauma. Nevertheless, in contrast to hypoxic- or pathogen-induced lung injury, H₂S treatment appears to have no protective effect after blunt chest trauma.
authors.affiliation: Department of Trauma Surgery, University of Ulm, Germany. daniel.seitz@uniklinik-ulm.de
authors.forename: Daniel H
authors.initials: DH
authors.lastname: Seitz
authors.forename: Janine S
authors.initials: JS
authors.lastname: Fröba
authors.forename: Ulrike
authors.initials: U
authors.lastname: Niesler
authors.forename: Annette
authors.initials: A
authors.lastname: Palmer
authors.forename: Heinrich A
authors.initials: HA
authors.lastname: Veltkamp
authors.forename: Sonja T
authors.initials: ST
authors.lastname: Braumüller
authors.forename: Florian
authors.initials: F
authors.lastname: Wagner
authors.forename: Katja
authors.initials: K
authors.lastname: Wagner
authors.forename: Stefan
authors.initials: S
authors.lastname: Bäder
authors.forename: Ulrich
authors.initials: U
authors.lastname: Wachter
authors.forename: Enrico
authors.initials: E
authors.lastname: Calzia
authors.forename: Peter
authors.initials: P
authors.lastname: Radermacher
authors.forename: Markus S
authors.initials: MS
authors.lastname: Huber-Lang
authors.forename: Shaoxia
authors.initials: S
authors.lastname: Zhou
authors.forename: Florian
authors.initials: F
authors.lastname: Gebhard
authors.forename: Markus W
authors.initials: MW
authors.lastname: Knöferl
mesh_terms: D000280:Administration, Inhalation; D000818:Animals; D001831:Body Temperature; D016207:Cytokines / Q000378:metabolism; D006862:Hydrogen Sulfide / Q000008:administration & dosage*; D000860:Hypoxia; D007249:Inflammation; D007728:Kupffer Cells / Q000166:cytology; D008264:Macrophages / Q000378:metabolism; D008297:Male; D010587:Phagocytosis; D051381:Rats; D017207:Rats, Sprague-Dawley; D013154:Spleen / Q000166:cytology; D013898:Thoracic Injuries / Q000628:therapy; D013997:Time Factors; D014949:Wounds, Nonpenetrating / Q000378:metabolism*
chemical_list: D016207:Cytokines; D006862:Hydrogen Sulfide