Role Of Hydrogen Sulfide In Acute Lung Injury Induced By Lipopolysaccharide And Its Relationship With Nitric Oxide

Acute lung injury (ALI), is mainly characterized by diffusive injuries to lung epithelium and increased permeability of alveolar-capillary membranes caused by various factors, which lead to pulmonary edema and pulmonary closure. It expresses as distress of respiratory and refractory hypoximia clinically. There are many etiological factors that can evoke ALI/ARDS directly or indirectly. Lipopolysaccharide (LPS), the main component of the cell wall of gram-negative bacteria, is one of the most important factors causing pulmonary infection and systemic infection. LPS plays an important role in initiating inflammatory response through binding to its receptors and causing systemic inflammatory response syndrome (SIRS) which can induce ALI. ALI induced by LPS is an acute pulmonary inflammation response in the lung, in which the accumulation and activation of polymophonuclear neutrophil (PMN) and the release of a large number of inflammatory mediators and oxygen free radical are the key link. However, it remains incompletely illuminated the definite mechanism of LPS initiating inflammatory over-reaction and inducing ALI.Endogenous gaseous transmitters, a unique class of biomaterials in regulating homeostasis, are found to play important roles in a variety of physiological and pathological events. Up to now, three gaseous transmitters have been recognized, namely nitric oxide (NO), carbon monoxide (CO) and hydrogen sulfide (H2S). Mounting evidence confirmed the important role of NO and CO in ALI. H2S is the third to be included in the family of endogenous gaseous transmitters, following NO and CO. Researches about physiological functions and pathological effects of H2S became frequent only recently. It was proved that H2S participated in the regulation of neural function and vasomotion, as well as the pathogenesis of hypertension,...