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多器官功能障碍综合征猪模型内皮祖细胞的变化及作用

The change and effect of endothelial progenitor cells in pig with multiple organ dysfunction syndromes.

机构信息

Department of General Surgery, Changhai Hospital, The Second Military Medical University, Xiangyin Road, Shanghai 200433, PR China.

出版信息

Crit Care. 2009;13(4):R118. doi: 10.1186/cc7968. Epub 2009 Jul 15.

Abstract

INTRODUCTION

The dysfunction and decrease of endothelial progenitor cells (EPCs) may play a very important role in the initiation of organ dysfunction caused by trauma or severe sepsis. We aim to measure the number and function of EPCs in the progression of multiple organ dysfunction syndromes (MODS) caused by severe sepsis, which may help to understand the pathogenesis of MODS by the changing of EPCs.

METHODS

A total of 40 pigs were randomly divided into two groups, which were subjected to hemorrhagic shock, resuscitation and endotoxemia (experimental group, n = 20) or acted as a control (control group, n = 20). The number and function of EPCs including adhesive, migratory and angiogenesis capacities were analyzed at different times in both groups.

RESULTS

All the animals in the experimental group developed MODS (100%) and 17 of 20 animals (85%) died due to MODS; the incidence of MODS and death of the animals in the control group were 0% (P < 0.01). The number, migratory and adhesive capacities of EPCs decreased sharply in the animals of the experimental group corresponding to the increasing severities of MODS, but the angiogenesis function increased gradually until death. The decrease in function of EPCs preceded the decrease in number of EPCs. The decrease in number and function of EPCs occurred prior to the occurrence of MODS.

CONCLUSIONS

For the first time, it was observed that the number and function of EPCs decreased sharply in the progression of MODS and that it was prior to the occurrence of MODS. The decrease in number and function of EPCs may be one of the main pathogenic factors of MODS.

摘要

简介

内皮祖细胞(EPCs)的功能障碍和减少可能在创伤或严重败血症引起的器官功能障碍的发生中起非常重要的作用。我们旨在测量严重败血症引起的多器官功能障碍综合征(MODS)进展过程中 EPC 的数量和功能,这可能有助于通过 EPC 的变化来了解 MODS 的发病机制。

方法

将 40 只猪随机分为两组,两组均进行失血性休克、复苏和内毒素血症(实验组,n = 20)或作为对照(对照组,n = 20)。分析两组在不同时间 EPC 的数量和功能,包括黏附、迁移和血管生成能力。

结果

实验组所有动物均发生 MODS(100%),20 只动物中有 17 只(85%)因 MODS 死亡;对照组动物 MODS 的发生率和死亡率均为 0%(P < 0.01)。与 MODS 严重程度增加相对应,实验组动物 EPC 的数量、迁移和黏附能力急剧下降,但血管生成功能逐渐增加直至死亡。EPC 功能的下降先于 EPC 数量的减少。EPC 数量和功能的减少先于 MODS 的发生。

结论

首次观察到 EPC 的数量和功能在 MODS 的进展中急剧下降,并且早于 MODS 的发生。EPC 数量和功能的减少可能是 MODS 的主要发病机制之一。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/78bf/2750166/a8c8f8e65e17/cc7968-1.jpg

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