Mediators of XXXX induced by inhalation of bacterial endotoxin.

@entity558 @entity3009 @entity651 @entity358 @entity3352
The purpose of this study has been to further define the pathophysiologic aspects of @entity651 caused by the inhalation of endotoxin ( @entity558 ) using the morphometric approach to identify mediators that influence distal lung structure and function. Hamsters were divided into 3 groups 24 h prior to low dose @entity558 inhalation exposure (4 micrograms/m3 for 5 h): (1) pretreated with cobra venom factor to deplete complement in vivo, (2) pretreated with @entity3352 to block @entity3009 production, and (3) untreated control group. Both pretreatments abolished @entity558 -induced @entity358 as well as increases in capillary PMN and platelets seen in untreated control animals. Neither pretreatment had any effect on the @entity558 -induced decreases of other capillary leukocytes. Similarly, both methods of pretreatment failed to block increases in cellular interstitium of distal capillary septa induced with @entity558 alone. @entity558 provoked changes in capillary endothelium, especially seen as an increase in numerical density of endothelial pinocytotic vesicles. Decomplementation failed to alter this increase, but @entity3352 pretreatment blocked the effect. Neither treatment had any effect on their size. Low dose @entity558 inhalation also altered pulmonary capillary permeability to a 125I-BSA probe, which was found in significantly greater amounts in @entity558 -exposed lungs than in those of saline aerosol control lungs, but was not present in the air space as evidenced by negligible counts in bronchoalveolar lavages. It is evident that endotoxin on the epithelial side of the air-blood barrier leads to changes on the other side of that barrier.(ABSTRACT TRUNCATED AT 250 WORDS)
