硫化氢对脂多糖诱导离体大鼠肺动脉反应性变化的影响及其与一氧化碳的关系

发布时间：2019-02-19 21:47

【摘要】：目的:革兰氏阴性细菌内毒素的主要活性成分脂多糖(lipopolysaccharide , LPS) 可导致全身炎症反应综合征(systemic inflammatory response syndrome,SIRS)。肺脏是内毒素感染时最易受损的靶器官之一。LPS 介导的急性炎症反应在肺部可表现为急性肺损伤(acute lung injury,ALI),但其具体机制尚未完全阐明。以往对LPS 诱导的ALI 发病机制的研究主要集中于中性粒细胞(polymorphonuclear neutrophil,PMN)的激活及活性氧物质的产生等方面,但这并不能完全解释LPS 诱导的ALI 的发生机制。我室研究发现,LPS 可引起肺动脉内皮细胞损伤,从而使肺动脉反应性异常,肺循环稳态紊乱最终导致了ALI 的发生。探讨LPS 导致血管反应性紊乱的发病机制是当今该领域亟待解决的重要课题。众多因素参与血管反应性的调节,内源性气体信号分子以其具有持续产生,传播迅速,作用广泛等特点,对肺循环的作用与其它器官相比更具有特殊意义。已有研究发现,内源性气体信号分子一氧化氮(nitric oxide,NO)和一氧化碳(carbon monoxide,CO)均可参与LPS 诱导的血管反应性变化的调节,但LPS 导致血管反应性紊乱的机制尚不十分清楚,应用外源性小剂量NO 或CO 吸入疗法也并未收到十分理想的效果,是否还有人们尚未认识到的内源性气体信号分子参与LPS诱导的血管反应性变化的调节尚不得而知。最近,人们发现
[Abstract]:Aim: lipopolysaccharide (lipopolysaccharide, LPS), the main active component of gram-negative bacterial endotoxin, can lead to systemic inflammatory response syndrome (systemic inflammatory response syndrome,SIRS). Lung is one of the most vulnerable target organs in endotoxin infection. Acute inflammation mediated by LPS can be manifested as acute lung injury (acute lung injury,ALI) in lung, but its specific mechanism has not been fully elucidated. The previous studies on the pathogenesis of ALI induced by LPS mainly focused on the activation of neutrophils (polymorphonuclear neutrophil,PMN) and the production of reactive oxygen species, but this could not fully explain the mechanism of ALI induced by LPS. Our study found that LPS can cause pulmonary artery endothelial cell injury, thus make pulmonary artery reactivity abnormal, pulmonary circulatory homeostasis eventually leads to the occurrence of ALI. To explore the pathogenesis of vascular reactivity disorder caused by LPS is an important subject to be solved in this field. Many factors are involved in the regulation of vascular reactivity. The endogenous gas signaling molecules have the characteristics of continuous production, rapid propagation and extensive action, which is of special significance to the role of pulmonary circulation compared with other organs. It has been found that endogenous gas signaling molecules such as nitric oxide (nitric oxide,NO) and carbon monoxide (carbon monoxide,CO) are involved in the regulation of vascular reactivity induced by LPS. However, the mechanism of vascular reactivity disorder induced by LPS is still unclear. Exogenous low dose NO or CO inhalation therapy has not achieved a very satisfactory effect. It is not known whether there are endogenous gas signaling molecules involved in the regulation of vascular reactivity induced by LPS. Recently, people have discovered
【学位授予单位】：河北医科大学
【学位级别】：硕士
【学位授予年份】：2005
【分类号】：R363

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