【摘要】：目的:革蘭氏陰性細菌內毒素的主要活性成分脂多糖(lipopolysaccharide , LPS) 可導致全身炎癥反應綜合征(systemic inflammatory response syndrome,SIRS)。肺臟是內毒素感染時最易受損的靶器官之一。LPS 介導的急性炎癥反應在肺部可表現為急性肺損傷(acute lung injury,ALI),但其具體機制尚未完全闡明。以往對LPS 誘導的ALI 發(fā)病機制的研究主要集中于中性粒細胞(polymorphonuclear neutrophil,PMN)的激活及活性氧物質的產生等方面,但這并不能完全解釋LPS 誘導的ALI 的發(fā)生機制。我室研究發(fā)現,LPS 可引起肺動脈內皮細胞損傷,從而使肺動脈反應性異常,肺循環(huán)穩(wěn)態(tài)紊亂最終導致了ALI 的發(fā)生。探討LPS 導致血管反應性紊亂的發(fā)病機制是當今該領域亟待解決的重要課題。眾多因素參與血管反應性的調節(jié),內源性氣體信號分子以其具有持續(xù)產生,傳播迅速,作用廣泛等特點,對肺循環(huán)的作用與其它器官相比更具有特殊意義。已有研究發(fā)現,內源性氣體信號分子一氧化氮(nitric oxide,NO)和一氧化碳(carbon monoxide,CO)均可參與LPS 誘導的血管反應性變化的調節(jié),但LPS 導致血管反應性紊亂的機制尚不十分清楚,應用外源性小劑量NO 或CO 吸入療法也并未收到十分理想的效果,是否還有人們尚未認識到的內源性氣體信號分子參與LPS誘導的血管反應性變化的調節(jié)尚不得而知。最近,人們發(fā)現
[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
【學位授予單位】：河北醫(yī)科大學
【學位級別】：碩士
【學位授予年份】：2005
【分類號】：R363

【參考文獻】

相關期刊論文 前10條

1 杜軍保,陳曉波,耿彬,蔣宏峰,唐朝樞;硫化氫作為心血管信號分子的研究[J];北京大學學報(醫(yī)學版);2002年02期

2 杜軍保,閆輝,唐朝樞;新型氣體分子硫化氫參與高血壓形成機制[J];北京大學學報(醫(yī)學版);2003年01期

3 張春雨,杜軍保,卜定方,閆輝,湯秀英,斯琴,唐朝樞;內源性硫化氫在大鼠低氧性肺動脈高壓中的作用[J];北京大學學報(醫(yī)學版);2003年05期

4 齊建光,杜軍保,賈建峰,趙斌,張前進,李萬鎮(zhèn);低氧性肺動脈高壓大鼠肺血管結構及血漿一氧化氮的變化[J];北京醫(yī)科大學學報;1999年04期

5 戴鴻雁,凌亦凌,黃新莉,韋鵬;硫化氫在內毒素血癥大鼠動脈舒張反應性改變中的作用及其與一氧化氮的關系[J];河北醫(yī)科大學學報;2004年06期

6 陳曉波,杜軍保,耿彬,蔣宏峰,唐朝樞;感染性和內毒素性休克大鼠動脈組織中硫化氫的變化[J];基礎醫(yī)學與臨床;2003年04期

7 趙曉云,凌亦凌,谷振勇,孟愛宏,張君嵐;內源性CO/NO在內毒素休克大鼠主動脈低收縮反應中的介導作用[J];山東大學學報(醫(yī)學版);2002年02期

8 萬梅,凌亦凌,谷振勇,張君嵐,黃善生;內源性一氧化氮在內毒素引起的肺動脈高壓和肺損傷中的作用[J];生理學報;1999年01期

9 宮麗敏,杜軍保,石云,唐朝樞;一氧化碳對缺氧大鼠肺動脈平滑肌細胞增殖和凋亡的影響[J];實用兒科臨床雜志;2001年05期

10 馬占敏,劉秀蘭,杜軍保,郭志良;L-精氨酸對缺氧大鼠肺動脈膠原含量的影響[J];實用心腦肺血管病雜志;2000年03期

，

本文編號：2426909