国际呼吸杂志
國際呼吸雜誌
국제호흡잡지
INTERNATIONAL JOURNAL OF RESPIRATION
2012年
16期
1226-1229
,共4页
慢性阻塞性肺疾病%呼吸衰竭%机械通气%支气管肺泡灌洗%细胞
慢性阻塞性肺疾病%呼吸衰竭%機械通氣%支氣管肺泡灌洗%細胞
만성조새성폐질병%호흡쇠갈%궤계통기%지기관폐포관세%세포
Chronic obstructive pulmonary disease%Respiratory failure%Mechanical ventilation%Bronchoalveolar lavage%Cells
目的 慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)气道炎症特征是气道壁以淋巴细胞和肺泡巨噬细胞浸润为主,而管腔内则以中性粒细胞和巨噬细胞作用为主,为进一步了解COPD急性加重期气道炎症细胞的特点.方法 对23例COPD急性呼吸衰竭气管插管机械通气的患者进行支气管肺泡灌洗共32次,灌洗液进行白细胞计数及细胞分类分析.结果 23例患者中成功脱机拔除气管插管14例,住院死亡6例,病情恶化自动出院3例.23例患者共进行支气管肺泡灌洗32次,灌洗液回收量为(12.88±4.98)ml,回收率为(32,2±12.45)%;23例患者气管插管后即刻或次日行支气管肺泡灌洗,灌洗液白细胞计数中位数M为50×106/L;细胞分类中位数M为:上皮细胞18%、中性粒细胞60%、淋巴细胞2%、巨噬细胞8%、嗜酸粒细胞0%;其中14例顺利脱机拔管的患者,灌洗液白细胞计数中位数M为25×106/L;细胞分类中位数M为:上皮细胞19%、中性粒细胞60%、淋巴细胞1.5%、巨噬细胞6.5%、嗜酸粒细胞0%;住院死亡6例,灌洗液白细胞计数中位数M为50×106/L;细胞分类中位数M为:上皮细胞19%、中性粒细胞62%、淋巴细胞1%、巨噬细胞10%、嗜酸粒细胞0%;病情恶化自动出院3例,白细胞计数中位数M为100×106/L,细胞分类中位数M为:上皮细胞15%、中性粒细胞10%、淋巴细胞25%、巨噬细胞2%、嗜酸粒细胞2%;在14例顺利脱机拔管的患者中8例患者在病情好转脱离呼吸机前重复上述检查,白细胞计数中位数M为50×106/L,细胞分类中位数M为:上皮细胞11%、中性粒细胞52%、淋巴细胞1.5%、巨噬细胞4%、嗜酸粒细胞0%.结论 从支气管肺泡灌洗液所获得的COPD患者气道炎症细胞主要为肺泡巨噬细胞以及较多的中性粒细胞、T淋巴细胞,一部分患者还存在较多的嗜酸粒细胞,其中最主要的是中性粒细胞和肺泡巨噬细胞.这些细胞一方面通过吞噬异物和参与免疫调节发挥对肺的保护作用,另一方面又通过分泌细胞因子、蛋白酶等参与肺的损伤过程.COPD患者肺泡巨噬细胞及中性粒细胞在肺内大量聚集,肺防御机制被破坏,抗损伤功能减弱,巨噬细胞及中性粒细胞激活呈失控状态,释放过量炎性介质,导致肺损伤.COPD的患者各种致病因子长期得不到清除,自身修复和防御机能的平衡遭到破坏,下呼吸道无菌状态被扰乱,以致细菌在黏膜上定植.
目的 慢性阻塞性肺疾病(chronic obstructive pulmonary disease,COPD)氣道炎癥特徵是氣道壁以淋巴細胞和肺泡巨噬細胞浸潤為主,而管腔內則以中性粒細胞和巨噬細胞作用為主,為進一步瞭解COPD急性加重期氣道炎癥細胞的特點.方法 對23例COPD急性呼吸衰竭氣管插管機械通氣的患者進行支氣管肺泡灌洗共32次,灌洗液進行白細胞計數及細胞分類分析.結果 23例患者中成功脫機拔除氣管插管14例,住院死亡6例,病情噁化自動齣院3例.23例患者共進行支氣管肺泡灌洗32次,灌洗液迴收量為(12.88±4.98)ml,迴收率為(32,2±12.45)%;23例患者氣管插管後即刻或次日行支氣管肺泡灌洗,灌洗液白細胞計數中位數M為50×106/L;細胞分類中位數M為:上皮細胞18%、中性粒細胞60%、淋巴細胞2%、巨噬細胞8%、嗜痠粒細胞0%;其中14例順利脫機拔管的患者,灌洗液白細胞計數中位數M為25×106/L;細胞分類中位數M為:上皮細胞19%、中性粒細胞60%、淋巴細胞1.5%、巨噬細胞6.5%、嗜痠粒細胞0%;住院死亡6例,灌洗液白細胞計數中位數M為50×106/L;細胞分類中位數M為:上皮細胞19%、中性粒細胞62%、淋巴細胞1%、巨噬細胞10%、嗜痠粒細胞0%;病情噁化自動齣院3例,白細胞計數中位數M為100×106/L,細胞分類中位數M為:上皮細胞15%、中性粒細胞10%、淋巴細胞25%、巨噬細胞2%、嗜痠粒細胞2%;在14例順利脫機拔管的患者中8例患者在病情好轉脫離呼吸機前重複上述檢查,白細胞計數中位數M為50×106/L,細胞分類中位數M為:上皮細胞11%、中性粒細胞52%、淋巴細胞1.5%、巨噬細胞4%、嗜痠粒細胞0%.結論 從支氣管肺泡灌洗液所穫得的COPD患者氣道炎癥細胞主要為肺泡巨噬細胞以及較多的中性粒細胞、T淋巴細胞,一部分患者還存在較多的嗜痠粒細胞,其中最主要的是中性粒細胞和肺泡巨噬細胞.這些細胞一方麵通過吞噬異物和參與免疫調節髮揮對肺的保護作用,另一方麵又通過分泌細胞因子、蛋白酶等參與肺的損傷過程.COPD患者肺泡巨噬細胞及中性粒細胞在肺內大量聚集,肺防禦機製被破壞,抗損傷功能減弱,巨噬細胞及中性粒細胞激活呈失控狀態,釋放過量炎性介質,導緻肺損傷.COPD的患者各種緻病因子長期得不到清除,自身脩複和防禦機能的平衡遭到破壞,下呼吸道無菌狀態被擾亂,以緻細菌在黏膜上定植.
목적 만성조새성폐질병(chronic obstructive pulmonary disease,COPD)기도염증특정시기도벽이림파세포화폐포거서세포침윤위주,이관강내칙이중성립세포화거서세포작용위주,위진일보료해COPD급성가중기기도염증세포적특점.방법 대23례COPD급성호흡쇠갈기관삽관궤계통기적환자진행지기관폐포관세공32차,관세액진행백세포계수급세포분류분석.결과 23례환자중성공탈궤발제기관삽관14례,주원사망6례,병정악화자동출원3례.23례환자공진행지기관폐포관세32차,관세액회수량위(12.88±4.98)ml,회수솔위(32,2±12.45)%;23례환자기관삽관후즉각혹차일행지기관폐포관세,관세액백세포계수중위수M위50×106/L;세포분류중위수M위:상피세포18%、중성립세포60%、림파세포2%、거서세포8%、기산립세포0%;기중14례순리탈궤발관적환자,관세액백세포계수중위수M위25×106/L;세포분류중위수M위:상피세포19%、중성립세포60%、림파세포1.5%、거서세포6.5%、기산립세포0%;주원사망6례,관세액백세포계수중위수M위50×106/L;세포분류중위수M위:상피세포19%、중성립세포62%、림파세포1%、거서세포10%、기산립세포0%;병정악화자동출원3례,백세포계수중위수M위100×106/L,세포분류중위수M위:상피세포15%、중성립세포10%、림파세포25%、거서세포2%、기산립세포2%;재14례순리탈궤발관적환자중8례환자재병정호전탈리호흡궤전중복상술검사,백세포계수중위수M위50×106/L,세포분류중위수M위:상피세포11%、중성립세포52%、림파세포1.5%、거서세포4%、기산립세포0%.결론 종지기관폐포관세액소획득적COPD환자기도염증세포주요위폐포거서세포이급교다적중성립세포、T림파세포,일부분환자환존재교다적기산립세포,기중최주요적시중성립세포화폐포거서세포.저사세포일방면통과탄서이물화삼여면역조절발휘대폐적보호작용,령일방면우통과분비세포인자、단백매등삼여폐적손상과정.COPD환자폐포거서세포급중성립세포재폐내대량취집,폐방어궤제피파배,항손상공능감약,거서세포급중성립세포격활정실공상태,석방과량염성개질,도치폐손상.COPD적환자각충치병인자장기득불도청제,자신수복화방어궤능적평형조도파배,하호흡도무균상태피우란,이치세균재점막상정식.
Objective The characteristics of airway inflammation in chronic obstructive pulmonary disease (COPD) was the infiltration of the airway wall with lymphocytes and alveolar macrophages mainly,but there were mainly neutrophils and alveolar macrophages in airway lumens.Therefore,it was necessary to study more about the characteristics of airway inflammatory cells in COPD acute exacerbation period.Methods 23 patients intubated were treated with mechanically ventilation cause of acute respiratory failure with COPD,were done with bronchoalveolar lavage 32 times,and the lavage fluid were sent to the laboratory for analysis of leukocyte count and cell sorting.Results 14 of 23 patients were recovered and the trachea cannulas were pulled out. 6 of the patients were die,3 of the patients were discharged because of deterioration,23 patients were done with bronchoalveolar lavage 32 times.The recovery of lavage fluid was (12.88±4.98) ml,and the recovery rate was (32.2± 12.45) %,23 patients were lavaged immediately after intubation or in next day.The median of leukocyte count was 50× 106/L,and the median of cell sorting was:epithelial cells 18%, neutrophils 60%, lymphocytes 2%,macrophages 8%,eosinophils 0%,14 of the patients were recovered.The median of leukocyte count was 25× 106/L,and the median of cell sorting was:epithelial cells 19%,neutrophils 60%,lymphocytes 1.5 %,macrophages 6.5 %,eosinophils 0 %,6 of the patients were die.The median of leukocyte count was 50 × 106/L,and the median of cell sorting was:epithelial cells 19%,neutrophils 62 %,lymphocytes 1 %,macrophages 10%,eosinophils 0%,3 of the patients were discharged because of deterioration.The median of leukocyte count was 100 × 106/L,and the median of cell sorting was:epithelial cells 15%,neutrophils 10%,lymphocytes 25%, maerophages 2%, eosinophils 2%,14 of the patients were recovered and had spontaneously breathing without respirator.Before the trachea cannulas pulled out,that 8 patients were lavaged again,and the median of avage fluid leukocyte count was 50 × 106/L,the median of cell sorting was:epithelial cells 11 %,neutrophils 52 %,lymphocytes 1.5%,macrophages 4 %,eosinophils 0%.Conclusions The airway inflammatory cells in COPD from bronchoalveolar lavage fluid was mainly alveolar macrophage,and most of neutrophil and T lymphocytes,there were more part of the eosinophils in some patients,which the most important was neutrophils and alveolar macrophages.On one hand,these cells play a protective effect on lung by swallowing foreign bodies and immune regulation;on the other hand,these cells participated in lung injury by secreting cytokines,protease and others.For the COPD patients,lung defense mechanism and anti-injury function were damaged besause of alveolar macrophages and neutrophil accumulation in the lungs.Alveolar macrophages and neutrophil activation was out of control.Further,inflammatory mediators released excessively,leading to pulmonary injury.A variety of pathogenic factors could not be cleared in COPD patients for long-term,the balance between self-defense and repair function was destroyed.Lower respiratory tract asepsis wa disrupted,resulting in bacterial colonization in the mucosa.