Effects of N-acetylcysteine on pulmonary macrophage activity after intestinal ischemia and reperfusion in rats / with invited commentaries.
OBJECTIVE
Intestinal ischemia and reperfusion (I/R) is considered to be a critical and triggering event in the development of distal organ dysfunction after a variety of insults. It appears that activated leukocytes, especially polymorphonuclear granulocytes (PMNs), and reactive oxygen species are important mediators in the process. In the present study, the aim was to evaluate the behavior of pulmonary macrophages, acute lung injury and pulmonary endothelial permeability after intestinal I/R, together with potential alterations in pulmonary endothelial and epithelial ultrastructure and cellular membrane system integrity.


METHODS
Intestinal ischemia for 40 min was followed by reperfusion for 12 h in the rat. Macrophage uptake of radiolabeled bacteria, levels of pulmonary blood content assessed by radiolabeled red blood cells and pulmonary endothelial permeability of radiolabeled albumin, as well as pulmonary endothelial and epithelial ultrastructure and cellular membrane system integrity by the use of scanning electron microscopy and a tracer was evaluated after 12 h reperfusion. Treatment with the free radical scavenger N-acetylcysteine (NAC) administered prior to reperfusion was evaluated.


RESULTS
Overactivation of pulmonary macrophages was noted after intestinal I/R, as was a significant decrease in pulmonary blood content. No increase in pulmonary albumin leakage or increase in pulmonary water content was found after intestinal I/R as compared to controls. Treatment with NAC prevented against intestinal I/R-induced overactivation of pulmonary macrophages and a decrease in pulmonary blood content.


CONCLUSIONS
Reactive oxygen species may be involved in the regulation of pulmonary macrophage function and pulmonary circulation after intestinal I/R.
Börjesson
A
A
Department of Surgery, Lund University Hospital, Lund, Sweden.
Wang
X
X
Sun
Z
Z
Wallén
R
R
Deng
X
X
Johansson
E
E
Andersson
R
R
D000111:Acetylcysteine / Q000494:pharmacology*; D000818:Animals; D002199:Capillary Permeability / Q000187:drug effects; D004848:Epithelium / Q000648:ultrastructure; D015633:Extravascular Lung Water / Q000378:metabolism; D016166:Free Radical Scavengers / Q000494:pharmacology*; D007422:Intestines / Q000098:blood supply*; D008168:Lung / Q000648:ultrastructure; D008262:Macrophage Activation / Q000187:drug effects; D016676:Macrophages, Alveolar / Q000187:drug effects / Q000502:physiology*; D008297:Male; D010587:Phagocytosis / Q000187:drug effects; D011652:Pulmonary Circulation / Q000187:drug effects; D051381:Rats; D017207:Rats, Sprague-Dawley; D015427:Reperfusion Injury / Q000473:pathology / Q000503:physiopathology*
D016166:Free Radical Scavengers; D000111:Acetylcysteine