title: N-acetylcysteine (NAC) protects against acute kidney injury (AKI) following prolonged pneumoperitoneum in the rat.
abstract: BACKGROUND
  Acute kidney injury (AKI) following prolonged laparoscopy is a documented phenomenon. Carbon dioxide pneumoperitoneum induces oxidative stress. Previous experimental studies have shown that the antioxidant, N-acetylcysteine, protects the rat from AKI following ischemia-reperfusion. The aim of this study was to evaluate the effects of N-acetylcysteine (NAC) on rat renal function after prolonged pneumoperitoneum.
  
  
  METHODS
  Normal rats treated or not with NAC were submitted to abdominal CO(2) insufflation of 10 mmHg, at short and long periods of time of 1 and 3 h, respectively, and evaluated at 24, 72 h, and 1 wk after deinsufflation. Glomerular filtration rate (GFR) was measured by inulin clearance and oxidative stress was evaluated by serum thiobarbituric acid reactive substances (TBARS) RESULTS: No significant alterations in GFR were observed in normal animals submitted to the pneumoperitoneum of 1 h and evaluated after 24 h desufflation. With 3 h of pneumoperitoneum, a significant and progressive decrease in GFR occurred 24 and 72 h after desufflation with an increase in serum TBARS. GFR returned to normal levels a week later. In the NAC-treated rats, a complete protection against GFR drops was observed 24 and 72 h following 3 h of pneumoperitoneum associated with a decrease in TBARS.
  
  
  CONCLUSIONS
  These results suggest that NAC protects against acute kidney injury following prolonged pneumoperitoneum. These findings have significant clinical implications.
authors.affiliation: Department of Nephrology, University of São Paulo-School of Medicine, São Paulo, Brazil. trulu@usp.br
authors.forename: Antonio Carlos
authors.initials: AC
authors.lastname: Seguro
authors.forename: Luiz F
authors.initials: LF
authors.lastname: Poli de Figueiredo
authors.forename: Maria Heloisa M
authors.initials: MH
authors.lastname: Shimizu
mesh_terms: D000111:Acetylcysteine / Q000627:therapeutic use*; D058186:Acute Kidney Injury / Q000209:etiology* / Q000503:physiopathology / Q000517:prevention & control*; D000818:Animals; D000975:Antioxidants / Q000627:therapeutic use*; D002245:Carbon Dioxide / Q000008:administration & dosage; D005919:Glomerular Filtration Rate / Q000502:physiology; D007263:Infusions, Parenteral; D007444:Inulin / Q000378:metabolism; D007668:Kidney / Q000378:metabolism / Q000503:physiopathology; D008297:Male; D023421:Models, Animal; D018384:Oxidative Stress / Q000502:physiology; D011027:Pneumoperitoneum / Q000150:complications*; D051381:Rats; D017208:Rats, Wistar; D015427:Reperfusion Injury / Q000150:complications*; D017392:Thiobarbituric Acid Reactive Substances / Q000378:metabolism; D013997:Time Factors
chemical_list: D000975:Antioxidants; D017392:Thiobarbituric Acid Reactive Substances; D002245:Carbon Dioxide; D007444:Inulin; D000111:Acetylcysteine