Cardiopulmonary, histologic, and inflammatory effects of intravenous Na2S after blunt chest trauma-induced lung contusion in mice.

@article{Wagner2011CardiopulmonaryHA,
  title={Cardiopulmonary, histologic, and inflammatory effects of intravenous Na2S after blunt chest trauma-induced lung contusion in mice.},
  author={Florian Wagner and Angelika Scheuerle and Sandra Weber and Bettina Stahl and Oscar McCook and Markus W. Kn{\"o}ferl and Markus S Huber-Lang and Daniel H. Seitz and J{\"o}rg Thomas and Pierre Asfar and Csaba Szab{\'o} and Peter M{\"o}ller and Florian Gebhard and Michael K. Georgieff and Enrico Calzia and Peter Radermacher and Katja Wagner},
  journal={The Journal of trauma},
  year={2011},
  volume={71 6},
  pages={
          1659-67
        }
}
BACKGROUND When used as a pretreatment, hydrogen sulfide (H2S) either attenuated or aggravated lung injury. Therefore, we tested the hypothesis whether posttreatment intravenous Na2S (sulfide) may attenuate lung injury. METHODS After blast wave blunt chest trauma or sham procedure, anesthetized and instrumented mice received continuous intravenous sulfide or vehicle while being kept at 37°C or 32°C core temperature. After 4 hours of pressure-controlled, thoracopulmonary compliance-titrated… 

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References

SHOWING 1-10 OF 35 REFERENCES

Inflammatory Effects of Hypothermia and Inhaled H2S During Resuscitated, Hyperdynamic Murine Septic Shock

During anesthesia and mechanical ventilation, inhaled H2S exerted anti-inflammatory effects, which were at least in part independent of the nuclear transcription factor &kgr;B pathway, however, not amplified by adding deliberate hypothermia.

Inflammatory alterations in a novel combination model of blunt chest trauma and hemorrhagic shock.

The results suggest that the leading insult regarding the immunologic response is lung contusions, supporting the concept that lung contusion represents an important prognostic factor in multiple injuries.

Role of Hydrogen Sulfide in Severe Burn Injury-Induced Inflammation in Mice

Findings show for the first time the role of H2S in contributing to inflammatory damage after burn injury, as evidenced by MPO activity and histological changes in liver and lung.

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

In anesthetized and mechanically ventilated mice, inhaled hydrogen sulfide did not amplify the systemic hemodynamic and cardiac effects of hypothermia alone and may offer metabolic benefit during therapeuticHypothermia, possibly via the maintenance of mitochondrial integrity.

Hydrogen sulfide attenuates myocardial ischemia-reperfusion injury by preservation of mitochondrial function

It is demonstrated that the delivery of H2S at the time of reperfusion limits infarct size and preserves left ventricular (LV) function in an in vivo model of myocardial ischemia-reperfusion (MI-R) and that either administration of H 2S or the modulation of endogenous production may be of clinical benefit in ischemic disorders.

Effects of hydrogen sulfide on inflammation in caerulein-induced acute pancreatitis

Data provide evidence for anti-inflammatory effects of H2S based on its dosage used, and it was revealed that significant reduction of inflammation, both in pancreas and lung was associated with NaHS 10 mg/kg.

Effect of Hydrogen Sulfide in a Porcine Model of Myocardial Ischemia-Reperfusion: Comparison of Different Administration Regimens and Characterization of the Cellular Mechanisms of Protection

This study demonstrates that infusion of H2S is superior to a bolus alone in reducing myocardial necrosis after IR injury, even though some markers of apoptosis and autophagy were affected in both H 2S-treated groups.

Generation of endogenous hydrogen sulfide by cystathionine γ-lyase limits renal ischemia/reperfusion injury and dysfunction

The findings suggest that the synthesis of endogenous hydrogen sulfide by CSE is essential to protect the kidney against ischemia/reperfusion injury and dysfunction and aids in the recovery of renal function following ischemIA/rePerfusion.