Effect of N-acetyl-L-cysteine on lung ischaemia reperfusion injury in a porcine experimental model.
BACKGROUND
The purpose of the present study was to investigate the effect of N-acetyl-L-cysteine on lung ischaemia reperfusion injury.


METHODS
Nineteen pigs were used. Group I (n = 5) underwent sham operation, group II (n = 7) 90-min left-lung ischaemia followed by 180-min reperfusion. In group III (n = 7) N-acetyl-l-cysteine was given (160 mg/kg) during ischaemia into the pulmonary artery. Lung-functional and haemodynamic parameters were measured; serum and lung tissue samples were obtained and analysed for interleukin-10 and tumour necrosis factor-alpha. At the end of the reperfusion bronchoalveolar lavage was carried out from the ipsilateral lung and analysis for total protein, phospholipase-A(2) and platelet-activating factor acetylhydrolase was carried out. Histological specimens were graded (0-3) for alveolar oedema, interstitial thickening and leucocyte infiltration. Statistical analysis was by means of one-way analysis of variance and Kruskal-Wallis test.


RESULTS
There were no differences in haemodynamic parameters, serum and tissue interleukin-10 and tumour necrosis factor-alpha. Pulmonary compliance was decreased in groups II and III (P = 0.002 and P = 0.001, respectively) during ischaemia and reperfusion. Pulmonary vascular resistance was increased in group II (P = 0.051) during reperfusion. In group III total protein and platelet-activating factor acetylhydrolase were increased (P = 0.004 and P = 0.006, respectively) and phospholipase-A(2) was reduced (P = 0.002), indicating an indirect surfactant-protective effect. Interstitial thickening was excessive in group II (P = 0.001); however, alveolar oedema was reduced (P = 0.002) when compared with group III.


CONCLUSIONS
N-acetyl-L-cysteine when administered directly in the pulmonary artery showed no significant change in haemodynamic and functional lung parameters during ischaemia reperfusion; it does, however, have an indirect surfactant-protective effect.
Chamogeorgakis
Themistocles P
TP
Attikon Hospital Center, University of Athens, Athens, Greece. thchamogeorgakis@yahoo.com
Kostopanagiotou
Georgia G
GG
Kalimeris
Constantine A
CA
Kabouroglou
George I
GI
Kourtesis
Antonios N
AN
Routsi
Christine I
CI
Dima
Cleanthi C
CC
Toumpoulis
Ioannis K
IK
D000111:Acetylcysteine / Q000008:administration & dosage / Q000627:therapeutic use*; D000818:Animals; D004195:Disease Models, Animal; D016166:Free Radical Scavengers / Q000008:administration & dosage / Q000627:therapeutic use*; D007261:Infusions, Intra-Arterial; D016753:Interleukin-10 / Q000378:metabolism; D008170:Lung Compliance / Q000502:physiology; D054467:Phospholipases A2 / Q000378:metabolism; D010972:Platelet Activating Factor / Q000378:metabolism; D015427:Reperfusion Injury / Q000378:metabolism / Q000503:physiopathology / Q000517:prevention & control*; D013552:Swine; D014409:Tumor Necrosis Factor-alpha / Q000378:metabolism; D014655:Vascular Resistance / Q000502:physiology
D016166:Free Radical Scavengers; D010972:Platelet Activating Factor; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; D054467:Phospholipases A2; D000111:Acetylcysteine