Nitric oxide attenuates interleukin 2-induced lung injury.
BACKGROUND
The pathogenesis of interleukin (IL) 2-induced vascular leak syndrome may be related to neutrophil-mediated endothelial injury. Nitric oxide inhibits neutrophil superoxide anion synthesis and adherence to endothelial cells. The role of systemic nitric oxide in preventing IL-2-induced lung injury was studied in an experimental model.


METHODS
Sprague-Dawley rats (seven per group) were randomized to control, IL-2 treatment (1 x 10(6) units), and IL-2 with sodium nitroprusside 0.2 mg/kg. Lung injury was measured by estimation of extravascular lung water (wet:dry weight) and bronchoalveolar lavage (BAL) protein concentration, and by histological findings. Neutrophil infiltration was evaluated by measuring myeloperoxidase activity and BAL neutrophil concentration.


RESULTS
IL-2 produced significant lung damage characterized by leucocyte sequestration (increased myeloperoxidase and BAL neutrophil concentrations), pulmonary congestion and microvascular protein leakage (increased wet:dry weight ratio and BAL protein concentration). This injury was reduced significantly by the addition of sodium nitroprusside, the nitric oxide donor.


CONCLUSIONS
Nitric oxide reduces IL-2-induced lung injury.
Bouchier-Hayes
D
D
Department of Surgery, Royal College of Surgeons in Ireland, Beaumont Hospital, Dublin, Ireland.
Abdih
H
H
Kelly
C J
CJ
Barry
M
M
Redmond
H P
HP
Burke
P
P
Tanner
A
A
Bouchier-Hayes
D J
DJ
D000818:Animals; D007376:Interleukin-2 / Q000009:adverse effects*; D008168:Lung / Q000187:drug effects* / Q000201:enzymology; D008297:Male; D009504:Neutrophils / Q000502:physiology; D009569:Nitric Oxide / Q000627:therapeutic use*; D009599:Nitroprusside / Q000494:pharmacology; D009195:Peroxidase / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley
D007376:Interleukin-2; D009599:Nitroprusside; D009569:Nitric Oxide; D009195:Peroxidase