Suspended animation inducer hydrogen sulfide is protective in an in?vivo model of ventilator-induced lung injury
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- 作者：Hamid Aslami (1)
André Heinen (1)
Joris J. T. H. Roelofs (2)
Coert J. Zuurbier (1)
Marcus J. Schultz (1) (3)
Nicole P. Juffermans (1) (3) - 关键词：Hydrogen sulfide ; Suspended ; animation ; like state ; Critical illness ; Acute lung injury ; Ventilator ; induced lung injury ; Inflammation
- 刊名：Intensive Care Medicine
- 出版年：2010
- 出版时间：November 2010
- 年：2010
- 卷：36
- 期：11
- 页码：1946-1952
- 全文大小：228KB
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André Heinen (1)
Joris J. T. H. Roelofs (2)
Coert J. Zuurbier (1)
Marcus J. Schultz (1) (3)
Nicole P. Juffermans (1) (3)
1. Laboratory of Experimental Intensive Care and Anesthesiology (L.E.I.C.A.), Academic Medical Center, Amsterdam, The Netherlands
2. Department of Pathology, Academic Medical Center, Amsterdam, The Netherlands
3. Department of Intensive Care Medicine, Academic Medical Center, room G3-206, Meibergdreef 9, 1105 AZ, Amsterdam, The Netherlands
文摘
Purpose Acute lung injury is characterized by an exaggerated inflammatory response and a high metabolic demand. Mechanical ventilation can contribute to lung injury, resulting in ventilator-induced lung injury (VILI). A suspended-animation-like state induced by hydrogen sulfide (H2S) protects against hypoxia-induced organ injury. We hypothesized that suspended animation is protective in VILI by reducing metabolism and thereby CO2 production, allowing for a lower respiratory rate while maintaining adequate gas exchange. Alternatively, H2S may reduce inflammation in VILI. Methods In mechanically ventilated rats, VILI was created by application of 25?cmH2O positive inspiratory pressure (PIP) and zero positive end-expiratory pressure (PEEP). Controls were lung-protective mechanically ventilated (13?cmH2O PIP, 5?cmH2O PEEP). H2S donor NaHS was infused continuously; controls received saline. In separate control groups, hypothermia was induced to reproduce the H2S-induced fall in temperature. In VILI groups, respiratory rate was adjusted to maintain normo-pH. Results NaHS dose-dependently and reversibly reduced body temperature, heart rate, and exhaled amount of CO2. In VILI, NaHS reduced markers of pulmonary inflammation and improved oxygenation, an effect which was not observed after induction of deep hypothermia that paralleled the NaHS-induced fall in temperature. Both NaHS and hypothermia allowed for lower respiratory rates while maintaining gas exchange. Conclusions NaHS reversibly induced a hypometabolic state in anesthetized rats and protected from VILI by reducing pulmonary inflammation, an effect that was in part independent of body temperature.