Abstract

Background: The role of poly(ADP-ribose) synthetase (PARS) inhibitor 3-aminobenzamide on lung injury was investigated in endotoxin-induced sepsis in 21 male Wistar rats (250-300 g) allocated into three groups.

Methods: The control group, received intraperitoneal saline (1ml kg-1 : n=7); the second group, intraperitoneal endotoxin (Escherichia coli lipopolysaccharide 055:B5  10 mg kg-1 :n=7); the third group, intraperitoneal 3-aminobenzamide 10mg kg-1  and 1 ml kg-1  saline 10 min before endotoxin (n=7). Six hours later, rats were sacrified with overdose of anaesthetic. Bronchoalveolar lavage (BAL) of the right lung was performed and used for assey of protein concentration and neutrophil count. The wet/dry lung ratio of the left lower lobe was calculated. Intravascular neutrophils of the left lung were cleared out with saline and asseyed spectrophotometrically for myeloperoxidase activity. For statistical evaluation analysis of variance was used.

Results: When compared with controls, administration of endotoxin caused a significant increase in mean pulmonary myeloperoxidase activity which was associated with an increase in mean BAL neutrophil concentration and mean lung wet:dry weight ratios as an expression of pulmonary extravascular lung water and microvascular leakage of protein  The increase in these values were not significant in the endotoxin+3-AB group.

Conclusion: The results of this study show that endotoxin challenge  is associated with marked pulmonary injury and part of the anti-inflamatory  effect of PARS in this injury may be related to the reduction of neutrophil recruitment into the inflamatory site.

Key Words: Sepsis, 3-Aminobenzamide, Pulmonary injury