关于败血症休克发病机理假说的实验(1)  被引量:2

Experiment study on hypothesis concerning the pathogenesis of septic shock (1)

在线阅读下载全文

作  者:戴顺龄[1,2] 段金虹[1,2] 李春涛 陆媛[1,2] 桂怡[1,2] 张仪华 斯勤 程锦轩[1,2] 凌亦凌 万梅[1,2] 

机构地区:[1]中国医学科学院基础医学研究所中国协和医科大学基础医学部 [2]河北医科大学病理生理教研室

出  处:《中国急救医学》1999年第1期9-11,共3页Chinese Journal of Critical Care Medicine

摘  要:目的将CA均有明显增高而临床症状截然相反的败血症休克(S)与神经源性肺水肿(NPE)进行部分病理生理比较研究,以期从两者差别及S的特殊性中,揭示其发病机理。方法肺系数、CAP、CAWP、微循环观察、血浆ET-1、NO测定;SS时iNOSmRNA肺组织原位杂交、Northernbolt原位PCR、胞内Ca++、胞内IP1、IP2、IP3测定。结果部分生理学指标显示:交感、CA占优势的不是SS而是NPE,NPE时血管病理性收缩,EF-l增高明显;而S时血管有病理性扩张、NO增高明显,内皮细胞胞内Ca++、IP3增高,肺组织iNOSmRNA表达增强;而Ach、M受体抑制剂654-2能使上述异常状态减轻或消失,恢复正常状态。结论在S发病机理中,交感与副交感系统均被激活,在交感、副交感系统高水平失衡基础上,以Ach-NO为主导,NO与超氧阴离子结合成ONOO-,继而形成OH·+NO-2,对细胞产生强烈毒性,导致血管病理性扩张为主,结合多种细胞因子与介质的激活形成SS。Objective To explain the pathgenesis of septic shock(SS) through comparing with part indices of pathoplysiology of SS and neurogenic pulmonary edema (NPE). Methods Pulmonary factors, cervical artery pressure (CAP), pulmonary artery wedge pressure (PAWP),serum ET 1, nitric oxide and micro circulation were observed. In SS gene expression of iNOS m RNA was tested in pulmonary tissue and PCR in situ hybridization and Northern blot. ([Ca ++ ]),(i),(i),(i)were also tested. Results Part physiology indices show vascular pathogenic contracting and factor ET 1 are in a high level status in NPE, While in SS vascular pathogenic dilation and factor NO in a high level status just as [Ca ++ ]i and i. Express of iNOSmRNA significantly increased in pulmonary tissue. M acceptor suppressions and anticholinergic drugs such as anisodamine can abate these symptoms.Conclusion In the pathogenesis of SS sympathetic nervous system and parasympathetic nervous system are activated to disturb the balance in a high level status, Ach NO system hold predominant, NO combine OO - to be ONOO - and soon be OH·+NO which is much toxic to cells and induce vascular pathogenic dilation. So some cellular factors and transmitters are activated to form SS. [

关 键 词:败血症 休克 乙酰胆碱 一氧化氮 副交感系统 

分 类 号:R631.402[医药卫生—外科学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象