NEUTROPHIL-ASSOCIATED LUNG INJURY AFTER THE INFUSION OF ACTIVATED PLASMA

被引:22
作者
GIE, RP [1 ]
DOERSCHUK, CM [1 ]
ENGLISH, D [1 ]
COXSON, HO [1 ]
HOGG, JC [1 ]
机构
[1] UNIV BRITISH COLUMBIA,ST PAULS HOSP,PULM RES LAB,1081 BURRARD ST,VANCOUVER V6Z 1Y6,BC,CANADA
关键词
ZYMOSAN-ACTIVATED PLASMA; ACUTE LUNG INJURY; NEUTROPHILS; POLYMORPHONUCLEAR LEUKOCYTES; INDOMETHACIN; HYDROXYUREA; VASCULAR PERMEABILITY; COLLOIDAL CARBON;
D O I
10.1152/jappl.1991.70.6.2471
中图分类号
Q4 [生理学];
学科分类号
071003 ;
摘要
Previous studies from our laboratory have shown that the infusion of zymosan-activated plasma (ZAP) caused large numbers of neutrophils (PMN) to accumulate in the lung. Although PMN are known to be activated by ZAP, it is unclear whether PMN delayed in the lung by ZAP infusion actually cause lung injury. The present study was designed to examine this question by measuring airway epithelial and endothelial injury. Airway epithelial injury was determined by depositing a known dose of fluorescein isothiocyanate-labeled dextran in the lung and measuring its appearance in the blood, and endothelial injury was measured by injecting colloidal carbon and measuring its accumulation in the microvasculature of the lung. The data show that ZAP infusion caused a mild epithelial and endothelial injury that did not increase either extravascular water or protein. This injury could be prevented either by depleting the animals of PMN or by pretreating them with indomethacin. In addition, the effect of ZAP infusion could be partially restored by transfusing donor PMN into the PMN-depleted animals. We conclude that ZAP infusion produces a mild lung injury that is dependent on PMN and the products of the cyclooxygenase pathway of arachidonic acid metabolism.
引用
收藏
页码:2471 / 2478
页数:8
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